Term
| An neuron cell body is stimulated but no AP is fired. The membrane potential is then measured a distance X away from the stimulus. What could we expect the potential to be? |
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Definition
| We expect the passive response to decay with distance over a membrane. |
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Term
| An neuron cell body is stimulated an reaches threshold potential. The membrane potential is then measured a distance down the axon. What could we expect the potential to be? |
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Definition
| You would expect the membrane potential to be the same (in amplitude) as the action potential. There is no decay of response with distance. |
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Term
| What happens down the axon from a stimulus that is hyperpolarizing? |
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Definition
There is some delay due to capacitance but because hyperpolarization does not cause AP's to fire, it decays with distance from the point of stimulation like an excitatory passive response.
What is a passive response? |
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Term
| What is a passive response? |
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Definition
| A passive response does not activate ion channels within a cell and decays with distance from the point of stimulus. |
|
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Term
| What is an active response? |
|
Definition
Causing an AP
An excitatory response --> EPSP's cause nearby sodium channels to open which causes the activation of sodium channels in the neighboring sodium channels |
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Term
| True of False: The key portion of the neuron where action potentials are initiated is the dendrites. |
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Definition
False.
Dendrites are utilized in the propagation of depolarization due to the response of ligand gated channels. |
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Term
| What happens down the axon of a neuron from a stimulus that is depolarizing? |
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Definition
It depends on if the stimulus is great enough to cause an action potential. If it is than the signal is propagated at the same magnitude all the way down the axon.
The axon arrives at the most distance sites with increasing delay.
However, if the depolarization stimulus was not enough to trigger an action potential than the response will decay with distance from the stimulus site. |
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Term
The decay of passive responses down an axon occurs in what manner?
a) Additionally
b) By halves
c) Exponentially
d) Linearly
What other factor would influence this rate of decay? |
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Definition
C - decay is exponential.
This is due to the cable properties of the axon.
The "leakiness" of the (membrane/axon) influences the speed with which the stimulus decays.
The leakier the (membrane/axon), the more channels that are open and the faster the stimulus response will decay. |
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Term
| Comparison of two axons: one that is leaky and one that is not… Both are stimulated with a passive, excitatory stimulus that does not initiate an action potential then the membrane potential a certain distance away from the point of stimulus is measured. What would you expect? |
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Definition
Leaky membrane --> Ie more channels are open.
You would expect the passive stimulus to decay faster for this membrane (or axon)
Non-leaky membrane --> Fewer channels are open
You would expect the passive stimulus to decay but at a slower rate than that of the leaky membrane. |
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Term
| If you increase the size of an axon, what happens to the internal resistance? |
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Definition
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Term
| What are oligodendrocytes? |
|
Definition
A form of myelinating cells Found in the CNS.
Can wrap around multiple axons at the same time. |
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Term
|
Definition
A form of myelating cell that is found only in the PNS.
Can wrap around only one axon at a time + only one section of the axon. |
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Term
| What is the function of oligodendrocytes and schwann cells? |
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Definition
Schwann and Oligodendrocytes are myelinating cells of the PNS and CNS respectively.
They speed up transmission by increasing the resistance of the membrane and decreasing the membrane capacitance. |
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Term
|
Definition
The wrapping of an axon with another membrane (IE oligodendrocytes or schwann cells) which increase the insulation around the axon.
This increases the resistance and decreases the capacitance of the cell, making it so that signals travel faster overall. |
|
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Term
| What is capacitance related to? |
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Definition
It's related to
- the distance between the two conducting plates (Ie the distance between the two layers of the membrane)
- The area of the membrane. The larger the area, the larger the capacitance. (area of the membrane patch, overall area of cell membrane, etc) |
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Term
| How is it that increasing myelination decreases capacitance? |
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Definition
| By increasing the thickness of the cell membrane, you decrease the capacitance (IE you increase the distance between the inside and the outside of the plate, thereby decreasing capacitance). |
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Term
| What is "saltatory" transmission? |
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Definition
The passing of an AP from node to node along a nerve fiber instead of along the membrane itself.
To specify: this occurs in axons that are myelinated. The signal jumps from node of ranvier to node of ranver where there are the highest concentrations of sodium channels. |
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Term
| On an axon myelinated axon, where would you find the largest concentrations of sodium channels? |
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Definition
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Term
| What factors are altered to allow a signal to travel much faster down a myelinated axon than an unmyelinated one? |
|
Definition
Increasing myelination increases resistance.
It also decreases capacitance. |
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Term
| What is the name of a disease that is characterized by the demyelination of axons? What are the symptoms or effect of this? |
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Definition
Multiple sclerosis is the most common demyelinating disease.
Demyelination results in impaired conduction of action potentials + the potential to excite parallel axons that are also demyelinated. |
|
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Term
| What happens during multiple sclerosis? |
|
Definition
MS is an autoimmune (IE immune system attacks self) disease wherein the immune system causes the breakdown of the myelin sheath.
This results in:
1) Decrease in conduction velocity
2) Frequency related block --> occurs when there are several AP's together. If the Axon cannot handle the speed by which they are propagated than there may be a failure down the line when the AP's come too close together. |
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Term
| What are the problems that can be associated with demyelination? |
|
Definition
1) Crosstalk between demyelinated axons
1. If demyelination of two adjacent axons occurs then the AP's in one will cause AP's to propagate in both directions of the adjacent axon.
2) Demyelinated Conduction
1. Decreased conduction velocity
a. Due to decreased resistance and increased capacitance
3) Frequency-related block
a. The signal moves more slowly through the demyelinated portion of the axon, but it still moves at regular velocity through the myelinated portion. So signals coming at a high frequency may catch up to the preceeding AP's and this can cause a failure distally which presents as a loss of "spikes" in AP.
4) Total conduction block
a. No signal can propagate past this point.
5) Ectopic Impulse Generation
a. AP's arise spontaneously beyond the point of demyelination.
6) Increased mechanosensitivity
a. Ectopic AP's arise due to mechanical stimulation. |
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Term
| How can you cause an ectopic action potential? |
|
Definition
Through demyelination.
If you demyelinate an axon than they become more mechanosensitive which can cause an increase in ectopic AP's (IE AP's that do not originate from the axon hillock |
|
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Term
| What is an ectopic action potential? |
|
Definition
| An action potential that originates from somewhere along the axon rather then at the axon hillock |
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Term
| Is MS a disease that is continually causing damage to the nerves ? |
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Definition
No, it is episodic.
There will be an episode where an amount of demyelination occurs in some part of your brain that causes a specific type of symtpom.
Then there is partial remyelination but the area remains subject to misfunction. |
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Term
| What are the kinds of synapses? Can they be divided further? |
|
Definition
There are electrical and chemical synapses.
Chemical synapses can be divided further:
Inotropic receptors = Protein that allows for the movement of ions. The transmitter released from one cell will cause the opening of ion channels in the second cell. (ligand gated channels)
Metabotropic receptors = Causes a metabolic change by activating a secondary messenger within the cell. (Can be ion channels opening but point is there's a secondary messenger). |
|
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Term
| Inotropic receptors and metabotropic receptors are both what? |
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Definition
| types of chemical receptors |
|
|
Term
| The protein Connexon forms what type of membrane protein? |
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Definition
| A connexon is an assembly of 6-proteins called connexins that form a bridge called a gap junction between the cytoplasm of one cell and the cytoplasm of another. |
|
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Term
| Where are NT molecules synthesized? |
|
Definition
Small-molecule neurotransmitters are synthesized locally within the axon terminal.
Others that involve enzymes are usually produced in the golgi of the cell body and are transported down microtubules to the nerve terminal. |
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Term
| Describe the steps of an AP with respect to the NT's. |
|
Definition
1) NT's are synthesized and packaged into vesicles
2) An AP arrives at the postsynaptic terminal
3) Voltage-gated Ca++ channels open, Ca++ enters into pre-synaptic terminal.
4) Rise in [Ca++] triggers fusion of synaptic vesicles within the presynaptic terminal
5) NT's diffuse across the synaptic cleft and bind to specific receptors on the post-synaptic cell
6) Bound receptors activate the post-synaptic cell (Open channels, activate G-proteins)
7) NT's break down and are retaken up by the pre-synaptic terminal, or other cells, or diffuses away from the synapse. |
|
|
Term
| What are the systems implemented to stop synaptic response? |
|
Definition
Stopping synaptic response involved
1) NT reuptake (transporters take them from the extracellular space)
2) Enzymatic break down
3) Diffusion away from activation sites |
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Term
| Which NT causes the excitation of skeletal muscle cells? What type of receptor does it act through? |
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Definition
Acetylcholine is the NT that excites skeletal muscle.
It acts through a nicotinic receptor. |
|
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Term
| How does the NT acetylcholine slow HR? |
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Definition
The release of acetylcholine acts on metabotropic receptors. In this case, it is the "muscarinic acetylcholine receptor".
This binding of ACh to the muscarinic ACh causes the dissociation of Alpha-GTP (alone) and the beta/gamma sub unit (bound together) from the heterotrimeric G-protein.
The free beta-gamma sub-unit then binds to an inwardly rectifying K+ channel which causes membrane hyperpolarization and causes a decrease in heart rate. |
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Term
| Nicotinic and muscarinic receptors refer to what? |
|
Definition
Nicotinic and muscarinic receptors are both acetylcholine receptors.
Nicotinic receptors are found in skeletal muscle cells where they play a role in excitation and contraction
Muscarinic receptors are found in the heart where they play a role in slowing down heart rate. |
|
|
Term
| Where do you find connexon channels? |
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Definition
| At gap junctions. They are the structural units that make up the channels that gap junctions are composed of. |
|
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Term
| What are connexon channels? |
|
Definition
Two Connexon channels make up GAP JUNCTIONS.
Fairly large pores that allow not only the movement of ions but also small molecules. These move back and forth between the cells that are linked.
These channels can either be rectifying (preferential movement in only one direction) or reciprocal (can move just as easily in both directions). |
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Term
| An electrical synapse consists of what? |
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Definition
| An electrical synapse consists of one or more gap junctions channels permeable to small ions and molecules. |
|
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Term
| Describe the structure of the nicotinic ACh receptor? |
|
Definition
It is a pentamer, ie made up of 5 sub units. (Alpha1, gamma, alpha2, beta, delta)
Each sub unit is made up of 4 helical segments (M1-M4)
**you need to bind two Ach to activate (the binding pockets are between the alpha sub units and the gamma sub units) |
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Term
| Describe the structure of a connexon. What is it? |
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Definition
A connexon is half of a gap-junction channel.
A connexon is made up of 6 connexin sub units. |
|
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Term
| What does oligomeric mean? |
|
Definition
| It means a complex containing several kinds of sub units --> IE, contains alpha, gamma, beta, delta etc |
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Term
| What is the difference between homo-oligomer, hetero-oligomer, and pseudo-oligomer |
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Definition
Homo-oligomer ==> in reference to channels ==> channel can be made up of identical, distinct sub units.
Hetero-oligomer ==> channel can be made up of homologous but not identical sub units.
Pseudo-oligomer ==> channels can have several repetitive sub-unit like domains within a single polypeptide. |
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Term
| What is the channel structure of voltage gated sodium, calcium and potassium channels and Ca-release channel? |
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Definition
They are tetrameric structures (IE 4 sub units)
The sub units of the voltage gated channels (Na, Ca, K) are composed of 6 helical segments.
The Ca-release channel is composed of ___________ helical segments |
|
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Term
| What is the difference between a gap junction, a connexin and a connexon |
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Definition
A connexin is a single sub-unit of a connexon.
A single connexon makes up half of a gap junction.
Two connexons, from two different cells, bind together to form a gap junction, which is a pore that allows the movement of small ions and molecules between the cells. |
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Term
| If cell 1 is voltage clamped at -40mV ad cell 2 is voltage clamped at -80mV and the cells are connected through gap junctions… in which direction will current flow? |
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Definition
The current will flow from positive to negative.
Therefore, voltage will flow from cell #1 to cell #2 (from -40 to -80) |
|
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Term
| What is the difference between a propagation of an AP through a gap junction or through a chemical synapse? |
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Definition
Gap junction : Because there isn't a perfect connection between Cell 1 and Cell 2, whatever changes there are in the first cell cause changes in the second but not as great.
So an AP in cell 1 may not cause an AP in cell 2.
Chemical synapse: An AP causes the depolarization of the cell which causes the release of NT's which cause the depolarization in the second cell firing another AP (therefore conserving charge). |
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Term
What is the closest channel, genetically, to the Cx32 channel?
a) Rat Cx26
b) Rat Cx32
c) Chick Cx43
d) Xenopus Cx43 |
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Definition
| Rat Cx32 only differs by 4 Amino Acids. |
|
|
Term
True or false:
Different cells of the body all express the same connexin sub-units.
Therefore, there is only one type of connexin within the body. |
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Definition
FALSE.
Different cells of the body express different types of connexins.
Therefore, there are many different types of connexins within the body |
|
|
Term
| What are the most common examples of cells that are connected through gap junctions? |
|
Definition
1) Cardiac cells
2) Glial cells
3) Smooth muscle cells (?) |
|
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Term
| Individual connexon (1/2 a gap junction) have recently been linked to what other functions? |
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Definition
| Could be involved in the secretion of substances such as ATP and glutamate from glia to act on neighboring neurons. |
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Term
| Why is the squid axon so important to modern science? What is the function of the large axon within the squid and how does it influence its behavior? |
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Definition
The presynaptic terminal of the axon is 1,000,000x larger than those in our brains. It also has connections to different nerves that branch into different parts of the squid.
**This synapse is involved in the squids escape response, so it's goal is to activate the number of axons which will activate the number of muscles that are involved in the escape response.
--> the larger diameter contributes to the increased speed at which this response can occur. |
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Term
| Neurotransmitter release depends on what? |
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Definition
| It depends on the depolarization of the pre-synaptic membrane as well as the influx of calcium (in order to fuse the vesicles with the membrane). Depolarization triggers the opening of the calcium channels (inward current). |
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Term
| If you decrease the concentration of extracellular sodium, what happens to the probability for AP's? |
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Definition
| Less extracellular sodium would decrease the likelihood for an action potential because there would be fewer ions to depolarize the cell. |
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Term
| What is the Nernst Potential for sodium, potassium and calcium? |
|
Definition
Sodium - +67
Potassium - -93
Calcium - +123
Chloride - -89 |
|
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Term
|
Definition
Cadmium, a divalent ion, can block calcium channels.
Cobalt is also another blocker of calcium channels. |
|
|
Term
| What ions can block calcium channels? |
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Definition
Cadmium or cobalt.
Basically, divalent ions. |
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Term
| If a cell experiences a voltage-step from -70 to +60, in what direction would we expect calcium to be moving and what would its driving force be? |
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Definition
You would expect calcium to be moving inwards, but slowly as it is closer to calcium's reversal potential.
Driving force:
The current of any particular ion = conductance for that ion (determined by number of channels that are open) x the driving force (how far away you are from equilibrium potential)
Or
I = G (V_m - E_x)
V_m - E_x = difference between membrane potential and equilibrium potential for that ion. |
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|
Term
If you block the presynaptic calcium channels than what will happen to the post-synaptic response?
a) It will be smaller in magnitude
b) It will not be present at all
c) It will be larger in magnitude
d) It will be half as much |
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Definition
If you block the presynaptic channels than there will be no post-synaptic response at all.
Answer is B. |
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Term
| What is a chelator? Give an example |
|
Definition
BAPTA is a chelator for Calcium.
A chelator is a molecule that binds other molecules.
Therefore, BAPTA is a molecule that binds calcium.
EGTA is another chelator for calcium but it is slower acting (does not bind as completely) |
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Term
| What does the fact that EGTA binding calcium does not completely inhibit postsynaptic response indicate? |
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Definition
| It indicates that the calcium is reaching the sensor that triggers release faster than it is being bound to EGTA. This means that the site of calcium entry must be extremely close (100nm) to the site that calcium binds to to trigger transmitter release. |
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Term
| Why is there a significant delay between calcium influx into the pre-synaptic cell and the post synaptic response? |
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Definition
1) The time it takes for diffusion across the synaptic cleft (temperature dependent, but does not cause a large effect)
2) The time that it takes for the binding mechanism of vesicles to occur (likely the largest contributor!) |
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Term
| What is the difference between the NT release at the neuromuscular junction or at those neuron synapses found in the brain? |
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Definition
- The amount of NT released at the NMJ is much greater than that found in the brain. This is so that there is a guarantee that there will be a firing of AP in the NMJ.
- The amount of NT released at the synapses in the brain is very minimal (often only one or a few quanta). It requires summation of inputs from several sources to fire action potentials. |
|
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Term
|
Definition
A molecule that blocks acetylcholine receptors.
Causes paralysis. |
|
|
Term
| What molecule blocks acetylcholine receptors? |
|
Definition
|
|
Term
The magnitude of postsynaptic potential will be greatest at what point of the cell?
a) Near the end plate
b) Near nucleus
c) It remains the same throughout the cell
d) It decays by halves as it moves away from the cell |
|
Definition
The magnitude for postsynaptic potential will be the greatest near the end plate.
It decays as it moves further away from the end plate. If the response was not enough to elicit an AP than it acts in the same way as a passive response (IE decays exponentially with distance). |
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Term
| If you reduce the concentration of extracellular concentration than what will happen to the post-synaptic response? |
|
Definition
The post-synaptic response will be decreased.
This is because there will be less calcium for the calcium-influx step, which will lead to fewer NT vesicles being fused with the membrane and overall fewer NT's diffusing across the synaptic cleft.
This will, in turn, result in a lower magnitude response from the post-synaptic cell. |
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Term
| If you increase the concentration of extracellular Mg, then fire an action potential, what will happen to the post-synaptic response? |
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Definition
It will be a lower magnitude response than one fired without a higher concentration of Mg++ present.
This is because Mg++ blocks calcium channels, leading to a smaller influx of Ca, a smaller number of NT's being released and a smaller post-synaptic response. |
|
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Term
|
Definition
Miniature end-plate potentials.
Occur spontaneously, not following directly after a stimulus.
The smallest possible MEPP correlates to the release on one quantum of neurotransmitter (IE release one vesicle). |
|
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Term
| What was used to demonstrate that the release of neurotransmitters occurs in a quantal fashion? |
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Definition
| The studies of MEPP's --> ie miniature end plate potentials. |
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Term
| The phenomenon of quantal release is explained by what? |
|
Definition
| Exocytotic fusion of the synaptic vesicles with the presynaptic membrane at the active zone. |
|
|
Term
| What are the types of synaptic vesicles? |
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Definition
Synaptic vesicle (appear clear) --> Smaller, 40-50nm
Dense core secretory granules (appear dark) --> Larger, 100-200nm |
|
|
Term
| What's the difference between synaptic vesicles and dense core secretory granules? |
|
Definition
Synaptic vesicles:
- Smaller (40-50nm)
- Transported from the golgi empty and are filled with non-peptide neurotransmitters at the nerve terminals
○ Those non-peptide neurotransmitters are synthesized at the nerve terminal
Dense core secretory granules:
- Larger (100-200nm)
- Filled with peptide neurotransmitters or hormones (at the golgi in the cell body)
○ The hormones/peptide NT's are synthesized in the plasma reticulum. |
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Term
| Describe the filling of a synaptic vesicle. Where does it occur and how is it accomplished? |
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Definition
The process occurs at the nerve terminal.
The process depends on a set of pumps. These pumps depend on a concentration gradient of protons.
In the vesicle there is a pump that uses ATP to pump H+ ions into the vesicle. There is then another pump that utilizes this established concentration gradient to exchange the protons for a neurotransmitter that will then be released at the active zone during neurotransmission. |
|
|
Term
|
Definition
| Where you take up a vesicle, refill and reuse it. |
|
|
Term
| How can you experimentally detect exocytotic fusion ( the release of neurotransmitters ) using carbon fibre? |
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Definition
You impose a positive charge onto the carbon fibre.
When the neurotransmitter diffuses past the carbon fibre, some of the NT will react (undergo oxidation) when it comes into contact with the carbon fibre.
This transfer of electrons can be seen as an increase in the carbon fibres current. |
|
|
Term
| Which neurotransmitters can be experimentally oxidized using the carbon-fibre method? |
|
Definition
Serotonin
Norepinephrine
Adrenaline (epinephrine) |
|
|
Term
| Which molecule would hold more serotonin, a synaptic vesicle or a dense-core vesicle? |
|
Definition
| The dense core vesicle will hold more. It's larger than the synaptic vesicle. |
|
|
Term
| How can exocytotic fusion be detected? |
|
Definition
1) Using the carbon-fibre technique
2) By measuring rapid changes in the total membrane capacitance of a cell
1. Fusion of the granule (or vesicle) with the membrane results in discrete increase in the total cell surface area and endocytosis causes a decrease. |
|
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Term
|
Definition
A coat protein that serves as the external scaffolding during vesicle formation at the trans-golgi and endocytosis.
The coat proteins preassemble in the cytoplasm to form three-armed "triskelions"
Endocytosis:
Triskelions attach to one another, then indirectly to the surface of the membrane that is to be excised by binding to the cytosolic tails of membrane proteins.
Adaptins, an adaptor protein, mediates this binding.
The triskelions then pulls up the membrane into a spherical configuration.
Dynamin is the GTP-binding protein that pinches off the membrane. |
|
|
Term
|
Definition
| three-armed coat protein that serves as the external scaffolding during vesicle formation at the trans-golgi and endocytosis. |
|
|
Term
|
Definition
An adaptor protein attached to triskelions (clathrin) that mediate the binding to the cytosolic tails of membrane proteins.
the triskelions then pull up the mebrane into a sphericle formation, n then dynamin pinches off the membrane. |
|
|
Term
| Describe vesicle formation. |
|
Definition
Occurs at the trans-golgi membrane.
The protein Clathrin forms three armed structures called "triskellions".
Triskelions attach to one another, then attach indirectly to the surface of the membrane (that is to be excised) through the protein "adaptin", an adaptor protein.
Adaptin binds to the cytosolic tails of the membrane proteins.
The triskelions then pulls the membrane into a sphericle configuration.
Dynamin, a GTP-binding protein {GTPase}, then pinches off the membrane.
The triskelion coating must be lost before the vesicle is able to undergofusion. |
|
|
Term
| Where does vescicle formation occur? |
|
Definition
| At the trans-golgi membrane (creation) |
|
|
Term
|
Definition
Also called VAMP or vesicle-associated membrane protein
Important protein found on vesicles. |
|
|
Term
|
Definition
Important protein found on vesicles.
Thought to be a calcium sensor. Therefore, the diffusion event (which is calcium dependent) is triggered by this molecule binding to calcium. |
|
|
Term
|
Definition
| A protein that reacts with vesicular proteins (synaptobrevin and synaptotagmin) |
|
|
Term
|
Definition
| A GTPase that plays a role in the formation of the VAMP, |
|
|
Term
| What is the v-type H+ pump? |
|
Definition
| This is the pump that uses the hydrolysis of ATP to pump hydrogen ions into vesicles. |
|
|
Term
|
Definition
| A molecule that may have a role in the formation of the pore during vesicular fusion with the membrane. |
|
|
Term
|
Definition
| Important in mediating the attachment of the vesicle to the actin cytoskeleton (which holds it in place during fusion and diffusion). |
|
|
Term
| What are the membrane-associated proteins of synaptic vesicles? |
|
Definition
V-type H+ channels --> pump that uses the hydrolysis of ATP to pump hydrogen ions into vesicles.
Neurotransmitter transporter --> Transports H+ ions out of the cell and neurotransmitters into the cell
SV 2 --> Not very well understood.
VAMP (synaptobrevin) --> Part of the complex that drives exocytotic fusion
Rab-3 --> A GTPase that plays a role in the formation of the complex
Synaptotagmin --> Calcium sensor. Triggers the diffusion event when calcium is bound.
Synaptophysin --> role in the formation of the pore during vesicular fusion with the membrane.
Synapsin 1 --> Important in mediating the attachment of the vesicle to the actin cytoskeleton (which holds it in place during fusion and diffusion). |
|
|
Term
| What is NSF? What proteins interact with NSF? |
|
Definition
NEM-sensitive factor (protein).
SNAPs (soluble NSF attachment proteins) are the proteins that interact with NSF's. |
|
|
Term
| NSF's interact with what protein? What protein, in turn, interacts with the proteins that interact with NSF's. |
|
Definition
SNAP's (soluble NSF attachment proteins) interact with NSF's.
SNARE's (SNAP receptors) interact with SNAP's.
SNARES can be divided into two types:
v-SNARE's = the SNARE's on the vesicles.
T-SNARE's = the SNARE's on the target membrane. |
|
|
Term
| What types can SNARE's be divided into? |
|
Definition
V-SNARE's => SNARE's on the vesicles membranes
T-SNARE's => The SNARE's on the target membrane.
examples of T-snares --> Syntaxin and SNAP-25 (SyNaptic-associated proteins) |
|
|
Term
| What is the snare hypothesis? |
|
Definition
four key components:
(i) a vesicle membrane protein named v-SNARE,
(ii) a target membrane protein dubbed t-SNARE,
(iii) a cytosolic protein required for membrane fusion N-ethylmaleimide-sensitive fusion protein (NSF), and
(iv) adaptors for NSF termed SNAPs (soluble NSF attachment proteins) |
|
|
Term
| Describe the exocytotic release of synaptic vesicles. |
|
Definition
1) Vesicles w/ synaptotagmin ([Ca+] sensor) and synaptobrevin (a v-SNARE) move to the nerve terminal membrane, which contains syntaxin and SNAP-25 (both t-SNARE's)
2) Formation of the "core complex" ==> "SNARE hypothesis"
1. N-sec 1 dissociates from syntaxin.
2. This allows syntaxin and SNAP-25 to form a complex.
3. Distal end of synaptobrevin begins tow ind around the syntaxin/SNAP-25 complex, forming a ternary complex.
3) Tightening of Ternary SNARE complex
1. The three SNARE's (synaptobrevin {VAMP}, syntaxin, SNAP-25) continue to tighten, drawing the vesicle and presynaptic membranes into close apposition.
4) Fusion and Exocytosis
1. The entry of Ca++ and its binding to synaptotagmin triggers fusion
5) Disassembly of the ternary SNARE complex
1. Soluble alpha-SNAP binds to the ternary complex formed by the intertwined SNAREs
2. ^ promote the binding of SNF (an ATPase) which uses the energy of ATP hydrolysis to disassemble the three tightly wound SNAREs.
6) Vesicle undergoes endocytosis. |
|
|
Term
| What are botulinum toxins? What do they affect? |
|
Definition
Comes from Clostridium Botulinum
Botulinum toxins are endopeptidases
They cleave synaptobrevin, SNAP-25, or syntaxin.
"flacid paralysis" : Leads to paralysis of the face leading to paralysis of the respiratory muscles. |
|
|
Term
| What are tetanus toxins? What do they effect? |
|
Definition
Comes from Clostridium Tetani
Is an endopeptidase
Tetanus toxins cleave synaptobrevin (VAMP).
"rigid paralysis" : Disease causes muscle rigidity or spasmatic contractions. (LOCK JAW) |
|
|
Term
| Whats the key difference between when vesicles that contain endocrine molecules or vesicles that contain neurotransmitters |
|
Definition
Vesicles for neurotransmitter release: high concentrations
Vesicles for endocrine release: low concentrations |
|
|
Term
| What is NEM? What does it do? |
|
Definition
| N-ethylmaleimide --> blocks the vesicular traffic through the Golgi complex by blocking NSF. |
|
|
Term
| Describe the steps of endocytosis. |
|
Definition
Triskelions attach to one another, then indirectly to the surface of the membrane that is to be excised by binding to the cytosolic tails of membrane proteins.
Adaptins, an adaptor protein, mediates this binding.
The triskelions then pulls up the membrane into a spherical configuration.
Dynamin is the GTP-binding protein that pinches off the membrane by hydrolyzing GTP. It acts by wrapping around the neck and pinching off. |
|
|
Term
|
Definition
| Dynamin is the protein that is responsible for "pinching off" the vesicle as it reforms during endocytosis. |
|
|
Term
|
Definition
Refers to a gene that was identified from fruit flies (Drosophila).
There's a mutation in the gene for dynamin, a GTPase that is responsible for the "pinching off" of a vesicle by wrapping around its neck.
The mutation causes the GTPase to be unable to do its final step (the disconnection) so there are long necks that form but they are unable to disconnect.
Therefore, vesicles cannot be reformed and you run out of vesicles to use. This leads to paralysis. |
|
|
Term
| What is the action of ACh in the neuromuscular junction primarily terminated by? |
|
Definition
| Primarily terminated by the action of the degradative enzyme acetylcholinesterase (AChE) |
|
|
Term
| What is the reversal potential for acetycholine receptors? |
|
Definition
Around 0 mV.
The reason for this is because it is a non specific channel and therefore permeable to both K and Na, which have large driving forces in opposite directions. |
|
|
Term
| The activation of action potentials in central neurons depend primarily on what? |
|
Definition
Usually depends on summation or integration of multiple subthreshold EPSPs and IPSPs.
Therefore, uses spatial or temporal summation of EPSP's. |
|
|
Term
| What is the difference between spatial and temporal summation? |
|
Definition
Spatial summation --> when you have more than one excitatory input being activated at the same time, there will be a summation of responses (at the same time). Bigger depolarization in the dendrite which may be enough to fire an AP.
Temporal summation --> action potentials occur at a single input (axon) but can occur quickly enough that it is added onto the previous depolarization. NT is released in quick succession and can result in a summation to above threshold. |
|
|
Term
| What is the structure of the nicotinic ACh receptor? |
|
Definition
It is a pentameric structure --> IE made of 5 subunits.
`Sub units in order: Alpha, Gamma, Alpha, Beta, Delta
Each sub unit is made up of 4 trans-membrane spanning regions: M1,M2,M3,M4
**requires two acetylcholine receptors to be activated. Their binding sites are between the alpha's and gamma sub unit. |
|
|
Term
| How can the rate and pattern of action potentials fired at the presynaptic terminal effect its function? |
|
Definition
Low frequency firing:
- Localized and short lived increases in calcium. Causes the release of vesicles that are closely associated with the presynaptic membrane. (small vesicles with NT's)
High frequency firing:
- Multiple action potentials fired, occurs fast enough that a buildup of Ca+ occurs throughout the terminal. This causes the release of both the dense core vesicles and the synaptic vesicles. |
|
|
Term
| How will a high frequency of firing AP's effect the functions of a presynaptic terminal? |
|
Definition
When multiple action potentials are fired off at once, the intracellular concentration of calcium begins to build up.
When the [Ca] exceeds the ability of the pumps to remove it, Calcium floods throughout the terminal.
This causes the potentiation for interaction between the synaptotagmin (Ca+ sensor) on both types of vesicles (dense core vesicles and synaptic vesicles) and therefore initiation the exocytotic process for both. |
|
|
Term
| How will a low frequency of AP's being fired affect the function of a presynaptic terminal? |
|
Definition
| When action potentials are being fired far enough apart that the calcium channels, or pumps, that remove calcium from the intracellular space, then calcium does not delocalize very far into the intracellular space. Therefore, only initiating exocytosis for the vesicles that are nearest to the presynaptic membrane. |
|
|
Term
|
Definition
| The ability of the synapse (connection) between neurons to change in strength. |
|
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Term
|
Definition
It refers to something that can happen when you start firing AP's rapidly.
Rapid firing of AP's causes an increase in the [Ca] within the presynaptic cell. This increases the probability of release of individual quanta of neurotransmitter.
"facilitation of release": there's more release so there's a bigger response in the post synaptic cell.
*This is likely caused by a buildup of calcium within the cell, which stimulates the initiation of exocytosis for both dense core bodies and synaptic bodies. |
|
|
Term
|
Definition
A theory where a rapid train of action potentials causes a slow increase in synaptic strength which lasts for some time. Can be shorter term or last for days.
The increase in strength of nerve impulses along pathways that have been used previously. Can be short term or long term. |
|
|
Term
|
Definition
| A short-term decrease in synaptic strength resulting from the depletion of synaptic vesicles at active synapses |
|
|
Term
|
Definition
| slow train of action potential can cause, over time, a slow decrease in response. Can happen slowly and reach a new lower level of probability. |
|
|
Term
| What are the different kinds of short term synaptic plasticity? |
|
Definition
Facilitation
Potentiation
Depression
Habituation |
|
|
Term
| What happens to relative synaptic strength if you add curare to a bath, but input high calcium concentration? |
|
Definition
You will see depression.
The reason for this is because the amount of calcium may be so high that it initiates exocytosis to the point where there are no more vesicles left. This shows as depression. |
|
|
Term
| What experiments have been done on Aplysia Californica? |
|
Definition
Experiments for synaptic plasticity, habituation or learning.
They discovered the gill and siphon withdrawal reflex.
Touching the gill or the siphon causes the snail to withdraw those structures. It shows habituation because each time that you stimulate it, if you measure the response it gets smaller and smaller each time.
It also shows disabituation because if you apply a large shock to the tail after applying a small stimuli to the gill/siphon… it will begin reacting the same was as before habituation began.
(you can also use this to show classical conditioning because if you continue paring these stimuli together eventually you will be able to ilicit the tail-shock response from stimulating the gill/siphon.) |
|
|
Term
|
Definition
| If an animal has undergone habituation, but you give the animal a large shock of a stimulus than the habituation will disappear (IE the response will come back in a large way) |
|
|
Term
| If you continually stimulate a receptor, but over time the response decreases, it is a sign of what? |
|
Definition
It is a sign of habituation.
If you are stimulating the receptor several times, but are seeing a decrease in the response strength over time, than it is depression. |
|
|
Term
You want to use classical conditioning to train an Aplysia's gill and siphon withdrawal reflex. Would you
A) Pair a light stimulus with a strong stimulus with minutes in between
B) Pair a medium stimulus with a strong stimulus near immediately
C) Pair a chemical transmitter with a medium stimulus
D) Pair a chemical transmitter with a light stimulus |
|
Definition
Answer is A:
You would pair a small stimulus with a much stronger stimulus that the animal will definitely respond to, than eventually small stimulus will cause the same response as the big stimulus but without the presence of that strong stimulus. |
|
|
Term
| What is the most important condition for classical conditioning to work? |
|
Definition
That you must have a pairing of stimulus. This causes the largest response.
One strong one that will be guaranteed to cause a response and one weak one that will not. However, you stimulate with the weak response first, then the strong one.
Example:
Ringing the bell and then serving the food in the case of Pavlovs dogs. |
|
|
Term
| What is the non-associative type of synaptic plasticity? |
|
Definition
|
|
Term
| What is associative learning? |
|
Definition
| Where a gentle stimulus will initiate the large response that a large stimulus originally would have after they have been introduced together for long enough. |
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|
Term
A scientist touches the foot of a ferret and measures its retraction response each time. The ferret, after a number of stimulations, begins to withdraw its food less and less. What is this called?
If the scientist then pinches the ferrets tail, causing a drastic response, then repeats the process of touching the ferrets foot, they find that the magnitude of withdrawal is back to what it had been before the first experiment. What is this? |
|
Definition
It is called habituation.
A stimulus being applied over and over again results in a reduced response.
This is dishabituation! |
|
|
Term
| Long term synaptic plasticity is analogous to what? |
|
Definition
|
|
Term
| If you stimulate a neuronal pathway and then measure the response extracellularily, what are you actually measuring? Is there another way to do this to obtain a different type of result? |
|
Definition
You are measuring the response of a bunch of cells.
You can also measure the response in a single cell. |
|
|
Term
Cells A, C and G all connect onto another cell, E. E then connects onto B which then connects onto D, which then branches into H and I.
If a rapid train of action potentials occurred at cell A, what could happen? What other cells would be affected? |
|
Definition
A rapid train of potentials at cell A could result in synaptic plasticity --> that is a change in the strength of response.
For example, long term potentiation (memory or long term synaptic plasticity) is possible.
If you stimulate Cell A, then the cells that are attached to it (and downwards from there) are going to be influenced as well. So, since C and G are adjacent but not attached to Cell A, they don't experience the same effect. However, Cells E, B, D, H and I all would experience a degree long term potentiation.
Note that even though H and I are branches from D, they would both still be influenced because they are part of the same "pathway" whereas C and G are part of their own pathways. |
|
|
Term
| Where in the body are you likely to see long-term potentiation? |
|
Definition
At excitatory synapses within the brain. Long-term potentiation is thought to be a very important concept for memory formation.
It has been most extensively studied within the hippocampus, even though it can occur at many excitatory synapses |
|
|
Term
| In long term potentiation, is it the synapse or the cell that is modified? |
|
Definition
| The synapse is what changes. The cell remains the same. Therefore, it's the synapse being potentiated - not the cell itself. |
|
|
Term
| A neuron has many dendrites. Long term potentiation is produced within dendrite A, will the adjacent dendrite B also experience LTP? |
|
Definition
Dendrite A and dendrite B aren't part of the same pathway because they are separate from each other (and therefore receive separate stimuli) and only commonly attach at the cell body.
Therefore, dendrite B will not experience LTP. |
|
|
Term
| True or false: LTP requires activation of the presynaptic terminals at the same time as depolarization of the postsynaptic neuron. |
|
Definition
True.
LTP does require activation of the presynaptic terminals at the same time as depolarization of the post-synaptic neuron. |
|
|
Term
| LTP requires activation of the presynaptic terminals at the same time as depolarization of the postsynaptic neuron. How is this achieved? |
|
Definition
This can be caused by:
- Repetitive stimulation of one input
- Coincident activation of two or more inputs |
|
|
Term
|
Definition
| Associative LTP refers to the fact that LTP requires not only the activation of the presynaptic terminal but requires the activation of the presynaptic terminal paired with the depolarization of the post-synaptic neuron. |
|
|
Term
Two neuronal pathways are stimulated.
In one pathway, a series of fast AP's are fired at a pre-synaptic terminal. The response is measured at the post synaptic terminal, which is not depolarized.
In another pathway, a series of fast AP's are fired at a pre-synaptic terminal. The post synaptic terminal is depolarized.
In which would we expect to see LTP? |
|
Definition
| You would expect it from the latter, where the post-synaptic cell is depolarized at the same time as the response in the pre-synaptic neuron from the high-frequency stimulation. |
|
|
Term
| Release of glutamate when the post-synaptic cell is depolarized will cause what? What would happen if the post-synaptic cell was not depolarized? |
|
Definition
Release of glutamate when the post-synaptic cell is depolarized (IE more positive) will cause the activation AMPA channels but also the activation of NMDA channels.
If the cell were not polarized, then there would be an activation of AMPA channels but the Mg+ block would still be present on the NMDA channels until the cell depolarized to a more positive value, allowing for their opening (and the block to leave). |
|
|
Term
| How could glutamate lead to long-term potentiation? |
|
Definition
|
|
Term
| How much contribution could we expect to cellular depolarization by the NMDA channels when the cell is at -80mV. |
|
Definition
| You would expect little contribution from NMDA channels because they are activated at more positive membrane potentials. |
|
|
Term
| What are the types of ionotropic glutamate receptors and what are their functions? |
|
Definition
AMPA --> Permeable to K, Na and sometimes Ca (rare). Opens quickly (at fairly negative mV). Mediates the great majority of fast excitatory neurotransmission in the central nervous system.
NMDA --> permeable to K, Na and Ca. Opens slowly, but because of it's high permeability to Ca it is important in synaptic plasticity. |
|
|
Term
| Would we expect more AMPA channels to be open at -60 mV or at +10 mV? |
|
Definition
| You would expect there to be more open at -60mV. This is because the reversal potential for a non-specific ionotropic channel is near 0mV. |
|
|
Term
| At what membrane potential would we expect to see more NMDA channels activated? At -80mV or at -30mV? |
|
Definition
| You would expect it to be active at the more positive membrane potential, like those during depolarization. |
|
|
Term
| Which are more closely related? GABA and ACh receptors, glutamate and ACh? |
|
Definition
| GABA and ACh are more closely related than glutamate receptors are to either. |
|
|
Term
| What does ACh receptor, GABAa receptor, glycine receptor and the serotonin receptor (5-HT) all have in common? |
|
Definition
They're all ligand gated channels.
They are all composed of five sub units. |
|
|
Term
| What's the difference between the ACh receptor, GABAa receptor, Glycine receptor, Serotonin receptor (5-HT) and glutamate receptor? |
|
Definition
They're all ligand gated channels (similarity)
Glutamate is a 4-subunit structure, whereas the first are all 5-subunit structures.
Each sub unit of the petameric structures are composed of four transmembrane regions, m1-m4.
The sub units of the glutamate sub-units are composed of, technically, 3 trans-membrane regions because m2 only "dips" into the membrane (doesn't cross it entirely). |
|
|
Term
| How many sub units are ionotropic glutamate receptors composed of? |
|
Definition
| 4, but technically three since M2 only "dips" into the membrane and does not cross it. |
|
|
Term
| How many sub units are GABAa receptors composed of? |
|
Definition
|
|
Term
| How many sub units are glycine receptors composed of? |
|
Definition
|
|
Term
| Howm any sub units are serotonin receptors (5-HT) composed of? |
|
Definition
|
|
Term
| How many sub units are ACh receptors composed of? (nicotinic receptors) |
|
Definition
|
|
Term
Which is the oldest ligand gated channel, evolutionarily?
a) ACh receptors
b) Glycine receptors
c) Serotonin receptors
d) Glutamate receptors
e) Glycine receptors |
|
Definition
| Glutamate channels are the most ancient + come from a different evolutionary line. |
|
|
Term
Which are more closely related between GABA, glycine, glutamate and ACh receptors?
a) GABA and Glycine
b) ACh and GABA
c) Glutamate and ACh
d) Glycine and ACh
e) Glutamate and GABA |
|
Definition
The answer is A - GABA and glycine.
**ACh is more closely related to the serotonin (5-HT) receptors and glutamate receptors are not evolutionarily close to any of them because it has a different evolutionary lineage. |
|
|
Term
| What's the biggest difference (one of them) between GABA/Glycine receptors and serotonin/ACh receptors? |
|
Definition
Serotonin/ACh receptors ==> Cation selective channels.
GABA/Glycine receptors ==> Anion selective channels. |
|
|
Term
| Which major ligand gated channels are cation selective? |
|
Definition
| Serotonin(5-HT3R)/ACh receptors |
|
|
Term
| The very first evolutionary split for receptors (channels) was a split in what way? |
|
Definition
| It split them into cation selective channels and anion selective channels. |
|
|
Term
| Which major ligand gated channels are anion selective? |
|
Definition
|
|
Term
| Describe metabotropic glutamate receptors. |
|
Definition
| Composed of 7-transmembrane spanning regions. Does NOT form a channel as it initiates a g-protein induced cascade within the cell. |
|
|
Term
| Is glutamate an excitatory or inhibitory neurotransmitter? |
|
Definition
|
|
Term
| True or false: Fe2+ blocks NMDA channels from opening at relatively negative membrane potentials. |
|
Definition
False!
It is Mg+ that blocks the channel at relatively negative potentials. |
|
|
Term
| True or false: If a post-synaptic terminal is depolarized and the pre-synaptic terminal is stimulated to release glutamate, what can we expect from the post-synaptic potential? |
|
Definition
We would expect both the NMDA and the AMPA channels on the post-synaptic membrane to be activated.
This is because depolarization causes the post-synaptic cell to be positive enough to kick off the Mg+ blockade from the NMDA receptors, so they open (still after the AMPA channels). |
|
|
Term
| At what potentials does Mg+ block NMDA channels? |
|
Definition
| At relatively low or hyperpolarized potentials. |
|
|
Term
| GABA and Glycine both act by opening what type of channels? |
|
Definition
| They both open Cl- channels (are anion selective). |
|
|
Term
| Strychnine is found to block what? What does it cause? |
|
Definition
It blocks glycine receptors.
Shifts the balance of motor neurons towards excitation in the spinal cord and brain stem. |
|
|
Term
| Where are glycine receptors found in the body? |
|
Definition
| They are found in the spinal cord and brain stem. |
|
|
Term
| What is startle disease and what causes it? |
|
Definition
Startle disease is caused by defects in glycine receptors.
Defects in glycine receptors cause a shit in balance for motor neurons towards excitation from input in the spinal cord and brain stem.
Causes spasms of the muscles etc. Causes "startling" to happen very easily. |
|
|
Term
| Anion selective channels cause the influx of what ion? At what potential would these most likely be open and have the greatest driving force? |
|
Definition
Chloride, Cl- is the ion that is influxed.
In skeletal muscle cells, the reversal potential for Cl- is ~-89mV in most other cells its around -47mV.
Therefore, the greatest driving force would be achieved during depolarization (or right after depolarization) when a cell is at its most positive value.
This means that they are inhibitory, or repolarize the cell, or cause hyperpolarization. |
|
|
Term
| Glycine and GABA are inhibitory or excitatory? |
|
Definition
They're inhibitory.
They tend to cause inhibition or hyperpolarization. |
|
|
Term
| Which receptor is responsible for mediating the effects of barbituates and benzodiazepines? |
|
Definition
| GABAa receptor channels are responsible for mediating the effects of barbituates and benzodiazepines. |
|
|
Term
| Which receptor channels are the most important inhibitory receptors in the brain? |
|
Definition
| The GABAa receptor channels. |
|
|
Term
|
Definition
| A member of the barbituate family, increases inhibitory responses in GABA a receptors.. Stimulates GABAa receptors, increases the probability and duration that they will be open. Increases the magnitude of the IPSP response. |
|
|
Term
| Which portion of the sub unit of GABA (and other heteropentamer channels) lines the pore? |
|
Definition
| M2 domain lines the central channel pore. |
|
|
Term
| What does GABA stand for? |
|
Definition
|
|
Term
| What are barbituates? What do they affect? |
|
Definition
Barbituates are sleeping pills from the 60s -- therefore has sedative effect
They effect GABAa receptors (increases their inhibitory effect) |
|
|
Term
| What are benzodiazepines and what do the affect? |
|
Definition
Valium is an example of benzodiazepines. They are used as anticonvulsants, to decrease anxiety, and as sedatives.
Act on GABAa receptors. |
|
|
Term
True or false:
Barbituates and benzodiazepines are most effective when GABA is already bound to GABAa |
|
Definition
| True! They enhance the response to GABA when it is bound. |
|
|
Term
| By what mechanisms can you increase synaptic efficacy? Which is seen during LTP |
|
Definition
1) Causing a change in the presynaptic cell so you get more release of NT
2) Increasing sensitivity in the post-synaptic cell
LTP causes an increase in sensitivity in the post synaptic cell |
|
|
Term
| If a strong and weak stimulus are both applied to the cell so that one causes the depolarization of the post-synaptic cell, what can we ascertain will happen? |
|
Definition
| We can ascertain that the neuronal pathways for both the strong and weak stimulus will be potentiated. |
|
|
Term
| True or false: LTP is due to an increase in sensitivity to a NT (glutamate, for example) in the post-synaptic cell |
|
Definition
True.
LTP causes the insertion of AMPA receptors into previously "silent" post-synaptic terminals (IE terminals that previously only contained NMDA receptors). This results in the same number of stimulus being detected by a larger number of post-synaptic receptors. |
|
|
Term
| What occurs to the post-synaptic cell during LTP transduction? |
|
Definition
If you have a depolarization of the post synaptic cell, which occurs during a rapid train of AP's or stimulation from two different sources, then there will be an influx of calcium in the post-synaptic cell.
This will cause the binding of calcium to the enzyme "calclium/calmodulin dependent protein Kinase II (CaMKII) and nearby vesicles that contain AMPA receptors.
Those vesicles will then undergo exocytosis of the AMPA receptors from the vesicles.
CaMKII activates the AMPA receptors by phosphorylating them and/or promoting their insertion into the post synaptic membrane.
The binding of new AMPA receptors to the post-synaptic membrane increases its efficacy in detecting NT's from the Pre synaptic cell. |
|
|
Term
| What is the function of CaMKII? |
|
Definition
CaMKII = calcium/calmodulin Dependent Protein Kinase II --> enzyme involved in the activation of AMPA receptors by phosphorylating them.
Also involved in promoting the insertion of AMPA receptors into the post synaptic membrane. |
|
|
Term
| Which enzyme helps to promote the insertion of AMPA receptors into the post synaptic membrane? |
|
Definition
| Calcium/calmodulin dependent protein kinase II (CaMKII). |
|
|
Term
| What type of stimulus is required to cause LTD? |
|
Definition
| A low-frequency stimulus (as opposed to the high-frequency stimulus which causes LTP) |
|
|
Term
| Whats the difference in the stimulation of LTD or LTP? |
|
Definition
Long term potentiation: Large increase in intracellular calcium due to a high frequency of AP's lead to net activation of protein kinases and thus phosphorylation of proteins (ex: synaptic proteins modulating AMPA receptor channel).
Long term depression: Moderate increase in [Ca] due to low frequency stimulation activates (preferentially) protein phosphatases which dephosphorylate the same synaptic proteins as in the previous. |
|
|
Term
| Ionotropic receptors are what type of receptor? What is the ACh one called? |
|
Definition
They are ligand gated ion channels.
The ACh receptor is called a nicotinic receptor. In skeletal muscle this receptor leads to muscle contraction. |
|
|
Term
| True or false: Metabotropic receptors are faster and have briefer effects than those of ionotropic receptors |
|
Definition
False.
Metabotropic receptors have slower, longer lasting effects. This is due to interacts with g-protein and the cascade of proteins initiated thereafter. |
|
|
Term
| Describe the steps for muscarinic metabotropic receptor. Function? |
|
Definition
1) Binding of ACh to receptor protein on post-synaptic cell.
2) Release of Alpha(subunit)-GTP(energy molecule) + beta-gamma subunit complex
3) Beta-Gamma subunits bind to an inwardly rectifying Potassium channel causes hyperpolarization, slowing down heart rate. |
|
|
Term
| How describe the structure of a G-protein-coupled-receptor. |
|
Definition
Has seven transmembrane spanning regions.
With neurotransmitter binding site on the extracellular surface and the G-protein coupled on the intracellular surface.
When the neurotransmitter binds with the extracellular surface it causes an interaction between the transmembrane regions and the g-protein, causing a conformational change and leading to the dissassembly of the g-protein sub units. This then leads to further cascades of reactions. |
|
|
Term
| What are the names of the acetycholine g-protein-coupled neurotransmitter receptors? |
|
Definition
Muscarinic receptors
M1, M2, M3, M4, M5 |
|
|
Term
| What are the names of the glutamate g-protein-coupled neurotransmitter receptors? |
|
Definition
mGluR 1-8
m=metabotropic
Glu (glutamate) R (receptor) |
|
|
Term
| What are the names of the serotonin g-protein-coupled neurotransmitter receptors? |
|
Definition
|
|
Term
| What is the primary enzyme required for the creation of cAMP? |
|
Definition
|
|
Term
| Describe the G-protein-coupled signalling cascade |
|
Definition
(Note: G-protein is composed of Alpha, Beta, Gamma subunits)
1) The G-alpha subunit is an enzyme, GTPase, and at rest is bound to GDP.
a. It is activated when the receptor molecule is bound to the activated receptor molecule, at which point GDP is exchanged for GTP thereby breaking the two subunit complexes apart
2) As just stated when activated, the Beta/Gamma sub units split apart from the Alpha subunit, which is still bound to a GTP molecule.
a. Alpha subunit can be inhibitory/excitatory … will bind to adenylyl cyclase and will decrease or increase the conversion of ATP to cAMP.
b. The alpha/GTP molecule dephosphorylates itself, thereby terminating its own activity.
i. cAMP then activates Protein Kinase A
1) Protein Kinase A (PKA) then phosphorylates outwardly rectifying potassium channels (depolarization)
c. Beta-gamma subunit bind to g-protein activated channel -- an inward rectifying K channel (causes hyperpolarization) |
|
|
Term
| What is the substrate that is converted into cyclic AMP? |
|
Definition
|
|
Term
| What is the enzyme that converted ATP to cyclic AMP? |
|
Definition
|
|
Term
| What molecule power PKA's. what are PKA's? |
|
Definition
1 neurotransmitter activates 1 receptor
1 receptor activates several G-proteins -->
Those G-proteins break apart and stimulate adenylyl cyclase, converting ATP to cAMP
cAMP can activate multiple PKA molecules (protein kinase A)
PKA in turn phosphorylates potassium channels (increases the probability that they will be open) |
|
|
Term
| True or false: there are inhibitory as well as excitatory G-proteins |
|
Definition
True.
Alpha-GTP sub unit can be either inhibitory in that it can activate or deactivate adynylyl cyclase which converts ATP to AMP. |
|
|
Term
| What does membrane delimited mean? Give an example of it |
|
Definition
Wherein the activation of a G-protein can only lead to the activation of proteins that are within the same patch of membrane.
Example: G-protein breaking apart and activating both adynylyl cyclase (leading to the activation of an outwardly rectifying K channel) and activation of an inwardly rectifying K-channel, |
|
|
Term
| How is phospholipase C regulation? |
|
Definition
The alpha-GTP subunit of G-protein breaks off and activates (or deactivates, if inhibitory?) pospholipase C (PLC).
PLC catalyzes the breakdown of phosphoinasotol disphosphate (PIP2) into diacylglycerol (DAG) and Inatosol triphosphate (IP3)
DAG - activates protein kinase C .
IP3 - binds to the IP3 receptor on the smooth endoplasmic reticulum which stimulates the release of Ca++. |
|
|
Term
| True or false: divergent means that multiple NT's can affect a single receptor |
|
Definition
FALSE
Divergent: a single NT can act on multiple receptors which stimulate different responses |
|
|
Term
Norepinephrine can bind to
a) Alpha1, alpha2, alpha3, and beta1 subunits
b) Alpha 1, alpha 2 and beta sub units
c) Alpha 1, beta 1 and beta 2 sub units
d) Delta, gamma, beta, alpha sub units |
|
Definition
| B: norepinephrine can bind to alpha1, alpha2, and beta sub units. |
|
|
Term
| Describe the signal-transduction cascade for the binding of norepinephrine to alpha-1 subunit. |
|
Definition
1) Binding to Alpha-1 subunit
2) Alpha-GTP subunit break apart and binds to PLC (phospholipase C)
1. Phospholipase C breaks phosphoinasotol disphosphate (PIP2) into diacylglyceral (DAG) and trisphosphate (IP3)
IP3 binds to EP3 receptor on smooth endoplasmic reticulum, which stimulates the release of Ca++
DAG activates protein kinase C, which |
|
|
Term
| Describe the signal transduction cascade for the binding of NE with Alpha-2 |
|
Definition
Can take two pathways:
1) Alpha2 --> Galphai or Galpha0
2) Alpha2--> Galphai or Galpha0
a. The GTP-Alpha subunit binds to PLC, which breaks apart PIP2 into DAG and IP3.
b. DAG can go on to bind to PKC
c. *or can act directly on a potassium channel directly (1) |
|
|
Term
| Describe the signal transduction cascade for the binding of NE with Beta sub units |
|
Definition
Beta sub unit becomes stimulated, which causes the release of GTP-alphas subunit
That GTP-alpha(s) subunit activates adenylyl cyclase, which converts ATP to cAMP. |
|
|
Term
The afterhyperpolarization current is caused by what channel
a) I-current
b) Ca-activated K+ channels
c) Sodium channel
d) T-current Ca channels |
|
Definition
| Ca-activated K+ channels. |
|
|
Term
| If you wanted to increase the duration of an action potential, what would you want to activate/inhibit? |
|
Definition
You would want to depress K+ current.
This would increase intracellular Ca++ (cause influx Ca channels would be open longer).
As a result the post synaptic potential in cell b is increased. |
|
|
Term
| Which neurotransmitter systems are responsible for wakefulness and arousal? |
|
Definition
| Norepinephrine and serotonin |
|
|
Term
| Which neurotransmitter systems are responsible for mood and emotional behavior? |
|
Definition
|
|
Term
| Which neurotransmitter system does hallucinogenic drugs affect? Is there another drug that acts on the same system? |
|
Definition
Serotonin
Anti-depressants act on the same system |
|
|
Term
| Where does the dopamine system originate from? What is it involved in?? |
|
Definition
| Originates in the substantia nigra |
|
|
Term
| The raphe nuclei is associated with what neuronal structures and what neurotransmitters are associated with the pathway? |
|
Definition
Raphe nuclei is associated with the basal ganglia.
It's associated with the serotonin systems. |
|
|
Term
| What are the names of the NT pathways in the brain, what's the name of the nucleus cells + the NT they associate with. |
|
Definition
1) Lobus coerulus --> norepinephrine
2) Raphe nuclei --> Serotonin
3) Substantia nigra --> dopamine
4) Septal nuclei, nucleus basalis, and Pontomesenphalotegmental cholinergic complex |
|
|
Term
| Which neurotransmitter is associated with voluntary movement? What else could it be involved with? |
|
Definition
Dopamine.
It also is associated with addictions |
|
|
Term
Modulation
Give an example: |
|
Definition
Occurs when a transmitter or hormone influences the responsiveness of a channel or cell to other stimuli. Regulation of ion channels such that the cell changes responsiveness to other signals.
Norepinephrine example:
Inhibits calcium activated potassium channels, which decreases after hyperpolarization and supresses the frequency adaptation. **It creates a tonic pulse frequency. |
|
|
Term
In the control state, wherein there is no neurotransmitter present, would you expect to see
a) Phasic
b) Tonic
c) Aphasic
d) A combination of A and B |
|
Definition
|
|
Term
|
Definition
| Wherein there is a frequency spiking of action potentials at the beginning but adaptation as the depolarizing current pulse is maintained. |
|
|
Term
|
Definition
| Wherein the train of AP's is similar to a regular burst of AP's, but is sustained for much longer. |
|
|
Term
| True or False: Beta-Andrenergic stimulation inhibits Ca2+ current through through a cAMP-dependent mechanism |
|
Definition
| False: Beta-andrenergic stimulation ENHANCES Ca2+ current through cAMP-dependent mechanism. |
|
|
Term
|
Definition
| It is an agonist of b-andrenergic, which, when stimulated, causes a large increase in the amount of calcium current by increasing the probability of the channels being open. |
|
|
Term
Which NT (or secondary messenger) can best modulate an increase in calcium current
a) Serotonin
b) Acetylcholine
c) cAMP
d) Barium |
|
Definition
| cAMP causes an increase in the probability that calcium ion channels will be open. |
|
|
Term
Muscarine inhibits which current:
a) T-current
b) M-current
c) L-current
d) High-threshold K+ current |
|
Definition
| M-current, which is a low threshold K+ current. |
|
|
Term
| The inhibition of M-current results in what effect? |
|
Definition
| M-current inhibition results in depolarization and an increase in excitability. |
|
|
Term
| The activation of the muscarinic receptors will turn off what current? |
|
Definition
| m-current, which will cause the cell to depolarize - or start at a new, more positive membrane potential and therefore make it more excitable. |
|
|
Term
| Modulation of the M-current leads to what? |
|
Definition
Inhibition of the M-current causes depolarization and an increase in excitability.
When it's active, it causes hyperpolarization and reduces the chances for repetitive AP's. |
|
|
Term
| Describe the basic steps of neuronal communication, starting at an environmental stimulus |
|
Definition
Environmental stimulus, ->
Receptor molecule ->
Transduction channel ->
Receptor potential ->
Spire train/neurotransmitter release -> |
|
|
Term
Sensory transduction depends on
a) Post-synaptic potentials mediated by ligand-gated channels
b) Receptor potentials mediated thru effect of an enviro stimulus
c) Depends on frequency of transduction APs |
|
Definition
| B - receptor potentials mediated through the effect of an environment stimulus acting on a receptor molecule. |
|
|
Term
| What are the different classes of sensory transduction? |
|
Definition
1) Thermoreception
2) Mechanoreception
3) Chemoreception
4) Visual Transduction |
|
|
Term
| What are TRP channels and where were they first identified? |
|
Definition
| Transient receptor potential channels were identified as a mutation in the Drosophila fruit fly. It showed a transient response to a sustained visual stimulus. |
|
|
Term
TRP channels
How can they be modulated |
|
Definition
Non-selective cation channels, some are permeable to Ca
Often play central roles in sensory transduction pathways such as those involved in pain, itch, heat, taste and touch.
Modulated/activated by a wide range of stimuli: temperature, pH, mechanical stress, interactions with chemicals… secondary messengers |
|
|
Term
| What type of channel is responsible for the "hot" response from capsaicin? |
|
Definition
|
|
Term
| What are the names of the different TRP channels |
|
Definition
TRPC = classic
TRPV = vanilloid --> chem structure tht is part of capsaicin and a lot of different alkaloids.
TRPM = melastatin
TRPA = ankyrin |
|
|
Term
| What is the mean firing rate for cold or hot thermoreceptor responses, respectively? |
|
Definition
Cold --> slower mean firing rate
Hot --> higher mean firing rate |
|
|
Term
True or false:
Cold thermoreceptors experience the highest mean firing rate at temperatures below 10*C |
|
Definition
False;
Below 10* they stop firing. People experience numbness to cold past this point (works as an anesthetic) |
|
|
Term
| Thermosensation is likely mediated by |
|
Definition
|
|
Term
Please in the order or decreasing threshold:
TRPM8, TRPV4, TRPA1, TRPV3, TRPV1, TRPV2 |
|
Definition
| TRPA1 --> TRPM8 --> TRPV4 --> TRPV3 --> TRPV1 --> TRPV2 |
|
|
Term
Which TRP channels are heat sensitive?
a) TRPV3, TRPV4, TRPM8, TRPV2
b) TRPV1, TRPM8, TRPA1, TRPV2
c) TRPV1, TRPV2, TRPV3, TRPV4
d) TRPM8, TRPM8, TRPV2, TRPV3 |
|
Definition
| C - TRPV1-4 are heat sensitive. |
|
|
Term
| Which TRP channels are cold sensitive? |
|
Definition
|
|
Term
| Which TRP channel is stimulated by capsaicin |
|
Definition
|
|
Term
TRP channels are:
a) Voltage gated channels that respond to heat and cold
b) Mechanosensitive channels that respond to touch
c) Ligand gated channels
d) Ligand gated/voltage dependent channels that sense heat and cold |
|
Definition
| D - ligand gated and voltage dependent channels that respond to both heat and cold. |
|
|
Term
| True or false: In hearing, you're detecting mechanovibrations and converting them into an electrical signal? |
|
Definition
True.
There is a conversion of a mechanical signal into an electrical signal. |
|
|
Term
|
Definition
|
|
Term
| True or false: Hair cells are a type of neuron involved in the process of hearing |
|
Definition
| False, hair cells are modified epithelial cells |
|
|
Term
| Are hair cells exposed to the air? If not, what types of fluids are they exposed to and what are their general compositions? |
|
Definition
Hair cells are exposed to two fluid compartments:
Endolymph: High concentration of potassium, therefore more similar to intracellular fluid.
Perilymph: Similar to the extracellular fluid within the rest of the body |
|
|
Term
| The sensation of hearing depends on what kind of channels? |
|
Definition
| Mechanosensitive TRP channels |
|
|
Term
| Describe the structure of vestibular hair cells. |
|
Definition
Vestibular hair cell bodies are surrounded by support cells.
The cell itself is exposed to the endolymph and the perilymph.
On the side exposed to the endolymph, there are small structures called sterevilli and kinocillum. They are arranged by smallest stereovilli to the kinocillum, which is the tallest. They are all connected by something called "tip links".
The deformation of the stereovilli/kinocillum causes the tip lings to deform their membrane, stimulating TRP mechanosensitive channels to either open or close. |
|
|
Term
| What's the resting membrane potential in a vestibular hair cell? |
|
Definition
|
|
Term
| True or False: TRP channels are selective to Calcium |
|
Definition
| False. They're non-selective cation channels |
|
|
Term
| Which ion is intimately involved with the depolarization of hair cells? |
|
Definition
Potassium ions.
This is because the endolymph has a high potassium concentration |
|
|
Term
| Describe the mechanism behind the sensation of hearing. |
|
Definition
Vibrations from sound waves cause mechanodeformation of the stereovilli/kinocillum structures of hair cells.
Mechanodeformation towards the kinocillum = activation of TRPA1 channels.
Mechanodeformation towards the stereocilli = inactivation of TRPA1 channels.
Opening of TRPA1 channels causes an influx of potassium from the endolymph, therefore depolarizing the cell and allowing the influx of Ca+ ions through L-type calcium channels, which leads to NT release.
Note: no AP's are fired. Small oscillations in membrane potential are enough to influence the L-type Ca channels. |
|
|
Term
In the mechanisms for hearing, it is the following channel responsible for exocytosis
a) L-type Ca channels
b) T-type Ca channels
c) TRPA1 channel
d) TRPM1 channel |
|
Definition
Answer is A
L-type Ca channels are opened when the cell depolarizes. |
|
|
Term
| True or false: In the mechanism for hearing, the frequency of AP's produced by the hair cells determines the frequency of sound |
|
Definition
False
There are no AP's being fired by the hair cells.
They shift back and force, opening and closing TRPA1 channels which depolarize the membrane (small magnitude) which then opens L-type Ca channel, initiating the exocytosis of NT containing vesicles. This is how the message is conveyed. |
|
|
Term
| What is the name of the L-type channel involved in auditory sensory perception? |
|
Definition
| Alpha-1-D (1.3 of the L-type channels) |
|
|
Term
| Where are the mechanosensitive channels found on hair cells? |
|
Definition
| Near the tip, at the bottom of the tip links. However, it was Not seen on the kinocillium (the tallest structure) |
|
|
Term
| What are the primary taste qualities |
|
Definition
Salt, sour, sweet, bitter, and umami
Salt - Usually Sodium
Sour - acidity
Sweet - Sugars
Bitter -
Umami - amino acid |
|
|
Term
|
Definition
| The taste sensation for amino acids |
|
|
Term
| Taste receptor cells are what kind of cells? What other kind of sensory cell is similar to this? |
|
Definition
Modified epithelial cells
Hair cells are also modified epithelial cells |
|
|
Term
| What are the different types of papillae? Where are they found |
|
Definition
Found on the tongue:
Folate (with serous gland near its base) found on the sides, near the back of the tongue
Circumvallate is found at the back, on the top of the tongue
Fungiform is found on the top of the tongue around the front and along the sides (but not on the side, still on the top) |
|
|
Term
| Describe the structure of a taste bud |
|
Definition
At the top there is a "taste pore" which has microvilli extending into it.
Below that is a dense substance that separates the taste/supporting cells from the environment.
The taste and supporting cells lay next to each other in a bulb-type structure beneath the top layer.
Within the taste cells are sensory neuron synapses |
|
|
Term
| What common molecule can be used to stimulate umami receptors? |
|
Definition
|
|
Term
| How many taste cells does each taste bud contain? |
|
Definition
| 50-100 taste cells within 1 |
|
|
Term
|
Definition
Epithilium Sodium Channel
Involved in Salt and sour sensation
Salt: Is a leak channel that acts through the reversal potential for sodium. When the concentration of sodium outside the cell exceed the inside of the cell, then the sodium will begin leaking in through these channels. This causes a membrane depolarization which opens Voltage Dependent Ca+ channels, which begin exocytosis.
Sour: pH-dependent opening of a TRP channel leads to depolarization and neurotransmitter release. Influx of H+ ion through ENaC is also possible. |
|
|
Term
| Describe the detection of salty things |
|
Definition
| When the concentration of sodium outside the cell exceed the inside of the cell, then the sodium will begin leaking in through ENaC. This causes a membrane depolarization which opens Voltage Dependent Ca+ channels, which begin exocytosis. |
|
|
Term
| Describe the detection of sour |
|
Definition
| Sour: pH-dependent opening of a TRP channel leads to depolarization and neurotransmitter release. Influx of H+ ion through ENaC is also possible. |
|
|
Term
| Describe the detection of sweetness |
|
Definition
Sweet perception depends on the binding of tastants to taste receptors.
Those receptors are G-protein coupled receptors. (Gustducin)
Activation of G-protein coupled receptor leads to activation of PLC and therefore the breaking down of PIP2 into IP3 and DAG.
IP3 causes a release of Ca+ from intracellular stores.
This increase of Ca activates Ca dependent TRP channels (TRPM5) leading to depolarization and transmitter release. |
|
|
Term
| Describe the chemodetection of amino acids |
|
Definition
Umami perception:
Umami perception depends on the binding of tastants to taste receptors.
Those receptors are G-protein coupled receptors. (Gustducin)
Activation of G-protein coupled receptor leads to activation of PLC and therefore the breaking down of PIP2 into IP3 and DAG.
IP3 causes a release of Ca+ from intracellular stores.
This increase of Ca activates Ca dependent TRP channels (TRPM5) leading to depolarization and transmitter release. |
|
|
Term
| Describe the detection of bitterness |
|
Definition
Bitterness perception:
Bitterness perception depends on the binding of tastants to taste receptors.
Those receptors are G-protein coupled receptors. (Gustducin)
Activation of G-protein coupled receptor leads to activation of PLC and therefore the breaking down of PIP2 into IP3 and DAG.
IP3 causes a release of Ca+ from intracellular stores.
This increase of Ca activates Ca dependent TRP channels (TRPM5) leading to depolarization and transmitter release. |
|
|
Term
| Which channels are involved in the detection of sweetness? |
|
Definition
ENaC (epithelial sodium channels)
TRPM5 (calcium-dependent TRP channel) |
|
|
Term
| Which channels are involved in the detection of sourness? |
|
Definition
pH-dependent TRP channel
ENaC |
|
|
Term
| True or false: the detection of umami is through the amino acids to ligand gated channels |
|
Definition
False.
Detection of umami is through a g-protein coupled cascade of reactions. |
|
|
Term
|
Definition
The g-protein that is specific for taste perception.
Specific for sweet, bitter and umami perception.
When it is activated it acts on phospholipase C, which in turn breaks PIP2 into IP3 and DAG.
IP3 acts on the IP3 receptor on the endoplasmic reticulum which causes it to open and allow calcium to enter into the cell.
Increase in intracellular calcium leads to activation of exocytotic release.
Membrane depolarization also leads to release of calcium from calcium channels. |
|
|
Term
| What is the name of the g-protein associated with olfactory perception |
|
Definition
|
|
Term
| True or false: Olfactory receptor cells are modified epithelial cells and respond to gaseous odorants |
|
Definition
False
Olfactory receptor cells are neurons. They respond to odorants dissolved in mucous that surrounds the olfactory epithelium. |
|
|
Term
| True or false: olfactory cells are neurons that respond to odorants dissolved in mucous |
|
Definition
|
|
Term
| Describe the cellular mechanism of odor sensation |
|
Definition
Odorants that are dissolved within mucous that surrounds the olfactory epithelium, stimulates the odorant receptor cells on the receptor cilia.
Their stimulation activates the G-protein G_olf
G_olf in turn activates adenylyl cyclase, which increases cAMP
cAMP stimulates the opening of a cAMP-gated cation channel, which causes a depolarization,
which activates voltage gated calcium channels to increases intracellular Ca+
The increase in Ca+ causes the activates of Calcium dependent Cl- channels
The Cl- channels cause depolarization because they have a high intracellular concentration, so Cl- flows outwards.
**this creates a graded receptor potential |
|
|
Term
| What are the functional, photon-detecting cells of the visual transduction system? |
|
Definition
Rods and cones.
Rods are responsible for low light detection
Cones are most active in high light conditions and detect color |
|
|
Term
|
Definition
| A functional unit of the visual transduction system. Is most active in low light situations and is not sensitive to color. |
|
|
Term
|
Definition
| A functional unit of the visual transduction system. Is most active in full light and is sensitive to color. |
|
|
Term
| Describe the photoreceptor outer segment |
|
Definition
Cones: folding of outer cell membrane results in increase of cell membrane area
Rods: Disks (?) Check book… |
|
|
Term
| True or false: A vertebrate photoreceptor mediates signal by firing off a higher frequency of action potentials |
|
Definition
| False: a vertebrate photoreceptor mediates a response by hyperpolarizing the membrane and inhibiting response. |
|
|
Term
| How does a vertebrate photoreceptor response differ from that of an invertebrate photoreceptor? |
|
Definition
Invertebrate: the stimulation of light causes cell depolarization and the firing of action potentials.
Vertebrate: the stimulation of light causes cell hyperpolarization through the actions of a G-protein (rhodopsin) |
|
|
Term
| Photoreceptor outer segment |
|
Definition
| The part of the photoreceptor cells that are specifically adapted for detecting photons of light and converting it to an electrical signal. |
|
|
Term
| Describe the structure of the retina (cell layers starting from the outermost layer inwards) |
|
Definition
1) Pigment epithelium
2) Photoreceptor outer segments (rods and cones)
**** |
|
|
Term
| Describe the cellular mechanism behind phototransduction |
|
Definition
Before light stimulation (in the dark… Ie resting conditions):
--> under resting conditions, cGMP is in relatively high concentrations (DUE TO ACTIOSN OF GUANYLYL CYCLASE CONVERTING GTP TO cGMP)
--> cGMP causes the opening of non-selective cation cannels (influx of Na)
--> these cation channels tend to contribute to depolarization of the cell and contributes to the high resting membrane potential.
--> Cation ions entering the cell are balanced by potassium ions exiting the cells through potassium cells leaving the inner segment
During light stimulation:
Photon converts retinal molecule in rhodopsin from 11-cis-retinal to 11-trans-retinal.
This activates Opsin, a 7-Transmemb. Spanning g-protein coupled receptor whose conformational change in turn activates the G-protein transducin.
The alpha sub unit from the transducin G-protein then goes on to activate the enzyme phosphodiesterase which converts cGMP to GMP.
As the concentration of inracellullar cGMP reduces, the cGMP activates channels begin closing -- this leads to a hyperpolarization of the cell (as these channels normally contribute to depolarization). |
|
|
Term
|
Definition
It is a receptor protein that responds to light and is composed of a Retinal + opsin complex
Found on the surface of the disks in the outer segment of the rod.
During rest (in the dark) it contains 11-cis-retinal. When stimulated by light, it undergoes a conformational change and becomes 11-trans-retinal. This is the activation of rhodopsin (activation of G-protein). |
|
|
Term
|
Definition
| 7-transmembrane segment G-protein coupled receptor that is in a complex with a vitamin A derivitive called Retinol. When Retinol undergoes a conformational change from 11-cis-retinol to 11-trans-retinol this activates opsin and thereby activates the G-protein transducin. |
|
|
Term
|
Definition
G-protein that's activated by the conformational change that retinal undergoes when it interacts with light.
Transducin (beta/gamma?) activates a guanylyl cyclase, an a GTPase enzyme that converts GTP to cGMP. cGMP activates non-selective cation channels.
The Alpha-GTP sub unit of transducin in turn activates phosphodiesterase, which hydrolyzes cGMP into GMP. The decrease of cGMP deactivates the non-selective cation channels and results in the hyperpolarization of the cell. |
|
|
Term
| Rhodopsin is made up of what proteins? |
|
Definition
| Rhodopsin is a receptor protein that is composed of opsin, a g-protein coupled receptor, and retinal, a molecule which undergoes a conformational change and activates opsin. |
|
|
Term
| True or false: rhodopsin is a 7-transmembrane segment g-protein coupled receptor that activates transducin |
|
Definition
False!
Rhodopsin is a receptor protein composed of opsin and retinal.
Opsin is the 7-transmembrane segment g-protein coupled receptor that activates the g-protein transducin. |
|
|
Term
Myelination
a) Increases resistance
b) Decreases capacitance
c) A and B
d) Decreases transmission velocity
e) None of the above |
|
Definition
| C --> myelination increases the resistance by increasing the insulation… it also decreases the capacitance by increasing the thickness of the membrane layers. |
|
|
Term
|
Definition
| Occurs when two unmyelinated fibers that are parallel to each other interact. Ie the AP's in one of them elicits an ectopic AP's in the parallel axon. |
|
|
Term
|
Definition
Wherein a frequency of AP's moves more slowly through the demyelinated portion of the axon, but still at regulated velocity through the myelinated portion.
This causes signals at high frequencies to catch up to the preceeding AP's that are within the demyelinated portion. This can cause a failure distally, which presents itself as a loss of "spikes" of AP's. |
|
|
Term
|
Definition
- Smaller (40-50nm)
- Transported from the golgi empty and are filled with non-peptide neurotransmitters at the nerve terminals
○ Those non-peptide neurotransmitters are synthesized at the nerve terminal |
|
|
Term
| Dense Core Secretory Granules |
|
Definition
- Larger (100-200nm)
- Filled with peptide neurotransmitters or hormones (at the golgi in the cell body)
• The hormones/peptide NT's are synthesized in the plasma reticulum |
|
|
Term
|
Definition
Receptor is at peripheral ending (Ie skin).
Elongated peripheral axon, which travels in peripheral nerve
Cell body located in dorsal root ganglion.
Short central axon entering spinal cord
Can only be excited - and becomes excited when the first excitable adjacent portion membrane becomes activated. |
|
|
Term
| Autonomic nervous system origin, structure and location. |
|
Definition
Two neuron chain.
1) Preganglionic fiber originating in CNS and terminating on a ganglion
2) Postganglionic fiber originating in the ganglion + terminating on the effector organ |
|
|
Term
| Termination for ANS efferent neurons |
|
Definition
Effector organs
IE cardiac muscle, smooth muscle, exocrine and some endocrine glands |
|
|
Term
| Effect and Function of ANS efferent neurons |
|
Definition
Carries instructions from CNS to effector organs . (smooth muscle, tissues with gab junctions)
Postganglionic fiber either excites or inhibits. |
|
|
Term
| Somatic nervous system origin, structure and location |
|
Definition
| Cell body of motor neuron lays in the spinal cord with a long axon traveling in the peripheral nerve and terminating on the effector organ (skeletal muscle) |
|
|
Term
| Effect and function of somatic nervous system |
|
Definition
| Carries instruction from CNS to effector organs (skeletal muscle) but can only cause excitation. |
|
|
Term
The action of the NT that excites muscle cells is terminated primarily by:
a) Adynylyl cyclase
b) Guanylyl cyclase
c) Acetylcholycinesterase (AChE)
d) Acetylcholine Transferase |
|
Definition
|
|
Term
| Tetrodotoxin/saxitoxin block what |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| N-type Calcium channels (voltage gated 2.2 channels) |
|
|
Term
|
Definition
| P/Q-type calcium channels |
|
|
Term
| Tetanus/botulinum block what |
|
Definition
| Cleave synaptic proteins, prevents the release of NT's at the NMJ. |
|
|
Term
| Black widow spider venom does what |
|
Definition
| Causes an explosive release of ACh |
|
|
Term
| D-tubocurarine and alpha-bungorotoxin block what |
|
Definition
AChR
Acetylcholine receptors |
|
|
Term
| Amyotropic lateral sclerosis (ALS) |
|
Definition
Disease results from the degeneration of motor neurons.
Characterized by gradual loss of motor function.
Paralysis/death within five years |
|
|
Term
|
Definition
Disease characterized by muscle weakness brought on by an autoimmune response to the ACh receptors at NMJ.
Treatment requires the extension of the activity of ACh within the NMJ.
Drugs that contain enzyme acetylcholine esterase. Pesticides / sarin both block its breakdown as well. |
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Term
| Origin of the preganglionic fiber in sympathetic system. Origin of the postganglionic fiber? |
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Definition
Thoracic and lumbar regions of the spine
Sympathetic ganglion chain (near spinal cord) or collateral ganglia (about halfway between the spinal cord and effector organs) |
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Term
| Origin of the preganglionic fiber in the parasympathetic nervous system. Origin of the postganglionic fiber? |
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Definition
Brain and sacral region of the spinal cord
Terminal ganglia (in or near effector organs) |
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Term
| Length/type of nerve fiber found in symapthetic nervous system |
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Definition
Short cholinergic preganglionic fibers
Long adrenergic postganglionic fibers |
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Term
| Length/type of nerve fiber found in the parasympathetic nervous system |
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Definition
Long cholineric preganglionic fibers
Short cholinergic postganglionic fibers |
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Term
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Definition
| Acetylcholine as the neurotransmitter |
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Term
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Definition
| Norepinephrine as the neurotransmitter |
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Term
| Preganglionic neurofibers release what neurotransmitters? |
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Definition
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Term
| Sympathetic ganglion chain |
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Definition
| Location of the synapse for the sympathetic nervous system |
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Term
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Definition
| The cauda equina is a bundle of nerves occupying the spinal column below the spinal cord in most vertebrates that consists of nerve roots and rootlets attached to the spinal cord. It serves the legs.[ |
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Term
| How many pairs of spinal nerves are there? |
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Definition
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Term
| How many spinal nerves are there? |
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Definition
| There are 31 pairs, therefore there's 62 spinal nerves in all. |
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Term
| What region of the spine is the location for the pre-ganglionic neurons for the sympathetic nervous system? |
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Definition
| Either in the thoracic or lumbar region of the spine |
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Term
| What region of the spine is the location of the parasympathetic pre-ganglionic neurons? |
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Definition
| In the lower part of the brain (brain stem) or down in the sacral region. |
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Term
| What's the difference between the length in parasympathetic and sympathetic neurons? |
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Definition
Parasympathetic: preganglionic fiber is fairly long (Ie the ganglion is nearer to the effector organ than spinal cord)
Sympathetic: shorter, ganglion is close to the spinal cord
Also, chromaffin cells in the adrenal medulla release epinephrine. |
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Term
| What is the name of nicotinic acetylcholine receptor channel in skeletal muscle |
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Definition
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Term
| What is the name of the receptor that is sensitive to ACh on the postsynaptic membrane of the postganglionic neuron. |
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Definition
| N2-type nicotinic receptor |
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Term
| where are the functions of alpha-1 receptors? where are they found? |
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Definition
Found in most sympathetic target cells.
excitatory response, generalized arteriolar vasoonstriction... or contraction of smooth muscle. |
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Term
| where are alpha-2 receptors found? what do they do? |
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Definition
inhibitory response in the digestive tract.
causes a decrease in smooth muscle contraction. |
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Term
| where do you find beta-1 receptors and what do they do? |
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Definition
found in the heart and perform an excitatory function.
increases rate and strength of cardiac muscle contraction. |
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Term
| where do you find beta-2 receptors and what do they do? |
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Definition
found in skeletal muscle and in the smooth muscle in some blood vessels/organs.
vasodilation in skeletal muscle/heart/bronchioles as well as breakdown of glycogen in skeletal muscle. |
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Term
| the adrenal medulla is activated as part of what nervous system response? |
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Definition
| the adrenal medulla is activated as part of the sympathetic nervous system. |
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Term
| alpha-1 adrenergic agonists help with what condition? |
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Definition
| is used to treat nasal congestion |
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Term
| beta-adrenergic antagonists are used to treat what? |
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Definition
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Term
| beta-adrenergic agonists are used to treat what? |
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Definition
| to treat asthma as bronchodilators |
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Term
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Definition
| a muscarinic antagonist that is used to dilate the pupil for eye exams |
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Term
| where does atropine come from? |
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Definition
| belladonna, or "deadly nightshade" |
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Term
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Definition
when one neurotransmitters binds to several kinds of receptors, which initiate different responses.
Ex: ACh activating ionotropic as well as muscarinic receptors initiates a fast mediated response but also a slow one. |
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Term
| what type of receptor does ATP bind to? |
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Definition
P2x
nonselective cation current. |
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Term
NE binding to the alpha-1 adrenergic receptor will initiate a response in what g-protein?
What does it lead to the activation of? |
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Definition
Gq
leads to the activation of PLC. |
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Term
| neuropeptide Y binds to what receptor? |
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Definition
| Y1 receptor. causes an increase in calcium concentrations. |
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Term
| what does nitric oxide do and where is it produced? |
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Definition
it is produced by neuronal nitric oxide synthase.
produced in the neuron but also neighboring endothelial cell.
it activates guanylyl cyclase to convert GTP to cGMP. this leads to the relaxation of smooth muscle cells. |
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Term
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Definition
| vasoactive intestinal peptide (VIP) causes decrease in intracellular calcium and relaxation of smooth muscle. |
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