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Definition
| found in vertebrates, mediates electrical synapses, allowing current to flow between two neurons. Cytoplasmic connection bridge between two neurons. |
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Definition
| found in invertebrates, mediates electrical synapses, allowing current to flow between two neurons. Cytoplasmic connection bridge between two neurons. |
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Definition
| The coupling of two neurons electrically, via connected cytoplasms... |
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Definition
| The ratio of v2/v1 when current is passed into cell 1. It is always less than 1. >.3 is a very strong coefficient, while .01 or less is weak. |
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| non-rectifying current in electrical coupling |
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Definition
| This means that current flows equally well in either direction between two electrically coupled cells. |
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Definition
| When current cannot flow equally from cell 1-> cell 2 and from cell 2-> cell 1 in electrically coupled cells |
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| Protein gates in electrical coupling |
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Definition
| Each cell contributes 6 protein subunits to the gate. If the subunits are the same ,the junction is non-rectifying. The more different the isoforms of the subunits, the more rectifying the cell could be. |
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| primary connexion in adult brain |
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Definition
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| Oligodendrocytes and Schwann cells make this connexion |
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Definition
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Term
| Charcot-Marie Tooth Disease |
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Definition
| Demyelinating disorder caused by mutation in Cx32. In this disorder, nutrients are still being delivered to cells, killing the cells, making it harder to treat than MS. CMT1A involves mutations in the Chromosome 18 myelin protein PMP22. CMT1B involves mutaqtion in Chromosome 1, causing a missense mutation in myelin Po protein. |
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Definition
| Performed experiment with frog hearts, transferring what came out of first frog heart (chemically) to second one, and noticed a slowing of the second heart. This meant chemical signalling existed... |
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Term
| Acetylcholine's effect in the heart? Metabotropic or Ionotropic? Which ion conductance does it affect, and how? |
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Definition
| inhibitory in the heart, used to slow heartbeat. It has its effect by G-protein coupled receptors, and increase potassium conductance, hyperpolarizing the cell. |
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Term
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Definition
| The receptor found in the heart bound by Ach, which inhibits it |
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Term
| Effect of denervating vagus nerve on heartrate |
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Definition
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Term
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Definition
| ARea on muscle fiber on which there are Acetylcholine receptors, found on the NMJ |
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Term
| How Acetylcholine release can make a muscle fiber contract |
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Definition
| At the endplate of the NMJ, Ach depolarizes the fiber. This depolarization will spread electrotonically until it gets into the tubules. This causes a release of Calcium into the sarcoplasmic reticulum, causing contraction on the muscle fiber. |
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Term
| Large safety factor of Acetylcholine |
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Definition
| Such a large safety factor that even if the AP in fiber is blocked, the release of Ach can still result in about a 50 mV depolarization. Decrease AchR in the cell will not dramatically affect phenotype of muscle contraction until a certain point is reached |
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Term
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Definition
| Taking Achetylcholine and putting it in a pipette. Pushing it over the endplate region. Functions as passing positive current of a known amount through a pipette. A larger amount released results in a larger response. |
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Term
| Ach channels outside of the heart have a mixed cation conductance. Which ions, Equilibrium potential? What does this mean about relative conductances? |
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Definition
| Permeable to Na+ and K+. Eq. potential is around 0 mV, meaning that the channel is more permeable to Na+ than K+ since its closer to its eq. potential. |
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Term
| Experiment comparing the IV curves of cells (in TTX and TEA to prevent APs and show the passive qualities of the channel) with Ach and a control. |
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Definition
| Shows that there is a difference in conductance between no Ach and Ach, and the Ach is OPENING channels (Na+ and K+) |
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Term
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Definition
| Receptor will hold onto the Ach, but over time the channel closes and the response lessens. |
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Term
| Acetylcholine is formed by... |
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Definition
| Acetate + Choline with an ester linkage. |
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Definition
| Restricts the amount of Ach that gets liberated to the receptor, limits the Ach getting through, and shortens the time it is available |
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Definition
| Nerve gases - kill you by slowing down heart since AchE is inhibited, which is normally limiting the slowing effect Ach has. |
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Definition
| Drug that acts as competitive antagonist on nicotinic AchRs. It is poisonous because it paralyzes respiration, but in smaller doses can be used in anesthesia to block muscle movement. |
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Term
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Definition
| Strongly, irreversibly binds to nAchRs. Causes death by paralyzing diaphragm. |
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Term
| Denervation supersensitivity |
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Definition
| If you cut the nerve, you can sometimes find Ach spread throughout the muscle. This can be prevented by blocking the AP. Seems to be regulated by Agrin, and is related to a series of postsynaptic and presynaptic moderators to spread out receptors |
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Term
| effect of injecting purified AchR from the electric eel into rabbits |
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Definition
| Rabbits died due to something similar to myesthenia gravis, where antibodies may go against the NMJ and fix receptors with AchEI. |
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Term
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Definition
| human disorder in which people make antibodies to their own acetylcholine receptors, degrading the structure of the NMJ. |
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Term
| How many Ach must bind to nicotinic Ach to open the channels? |
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Definition
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Term
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Definition
| The receptor is on the same molecule as the channel. Instant effect |
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Term
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Definition
| G-protein coupled receptor that eventually alters ion channel function through a second messenger cascade, ultimately changing ion channel formation. |
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Term
| Torpedo receptor protein conformation |
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Definition
4 transmembrane domains
9 different alpha subunits, many different beta. Multiple subtypes of this channel. |
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Term
| Function of slightly different types of receptors in brain? |
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Definition
| Allows for minor each subunit compositional difference to have a slightly different pharmalogical effect |
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Term
| Nicotinic receptors in the brain are affected primarily by which NT? |
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Definition
| Glutamate, and its effects are often seen presynaptically. |
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Term
| Many of the nicotinic receptors are located presynaptically. Why function does this serve? |
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Definition
| It allows the presynaptic neuron to alter transmission at the synapse. |
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Term
| Calcium's effect in the nervous system |
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Definition
| With normal levels of calcium, you will see a PSP followed by an AP. However, at lower levels of calcium, this decreases, and you are less likely to see AP. This is because Calcium affects vessicle release. |
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Term
Experiment:
Stimluate nerve in solution with 0 calcium. effect? |
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Definition
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Term
Experiment:
You have a solution with no Calcium. If you apply Calcium via pipette before depolarization, what happens? After? at the same time? |
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Definition
| You will ONLY see a PSP when calcium is applied at the TIME of depolarization. |
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Term
| Calcium in pre-synaptic terminal does what to the probability of vessicle release? |
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Definition
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Term
| "Mini" endplate potentials |
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Definition
| ARgued by Katz and Miledi to be single vessicles released by chance due to intracellular calcium. Also, they are slowed down when AchI is applied to post-synaptic cell suggesting the importance of postsynaptic activity in determining mini amplitude as well |
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Term
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Definition
| means that at rest, an EPSP will first evoke a response, and then a bigger response the second time... |
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Term
| Difference between short term facilitation and LTP |
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Definition
| LTP is providing a stable change in synaptic strength by changing the affinity/number of receptors on the post synaptic side. Short term facilitation is caused by an increase in the probability of vessicle release. |
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Term
Rules of quantal analysis:
define p, n, m, E, q |
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Definition
P = probability of the release of 1 quantum
n = store of readily releasable quanta
m = mean quantal contact...n * p
E = synaptic efficacy
Q = amplitude of 1 quantal response (1 vessicle) |
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Term
| How to solve for synaptic efficacy (E) |
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Definition
| E = m (# of quanta) * Q (amplitude of quanta) |
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Term
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Definition
| M = mean amplitude of syn. potential/mean amp. of mini |
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Term
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Definition
| Caused by a depletion in a neuron's readily releaseable pool |
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Term
| transmitters are placed where during neurotransmission? |
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Definition
| Inside the vessicle, tightly packed |
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Term
| How do Glutamate, Ach, GABA get into vessicle? |
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Definition
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Term
| vessicles are coated by what protein? |
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Definition
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Term
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Definition
| Created, docked, and then repackaged or degraded. Sometimes refilled and recycled. |
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Term
| Important proteins for the vessicle fusion process: |
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Definition
| 1) Synaptogrevin 2) synaptobogmin 3) Synaptophysin 4) transporter 5) pump 6) synapsin 7) cystine string protein |
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Term
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Definition
| Used to help transport vessicle and fuse it in the plasma membrane |
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Term
| Proteins that make up the SNARE complex and their functions |
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Definition
Syntaxin, SNAP-25 - vessicle proteins.
NSF, Piccolo, Basson - BIND to vessicle proteins. |
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Term
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Definition
| Blocks synaptic transmission by cleaving members of the SNARE complex. |
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Term
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Definition
BOTOX!
Paralyzes wrinkly muscles by preventing cutting neural transmission... |
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Term
| Effect of increase chloride conductances |
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Definition
| Will act to inhibit the neuron by lowering its Eq. potential. |
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Term
| glycine and its effects on channels |
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Definition
| Important amino acid and spinal cord inhibitor. Increases Cl- conductance, hyperpolarizing the cell. |
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Term
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Definition
| Rat poison. Blocks glycine |
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Term
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Definition
| Major inhibitory transmitter of the brain. |
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Term
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Definition
| Ionotropic receptors, usually inhibitory. Increases Cl- conductance. |
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Term
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Definition
| Metabotropic receptors that, as a result of G-protein coupking, increase K+ conductance. Always inhibitory. |
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Definition
| Enhances reaction to GABA. Strongly potentoate its effect by binding to specific sites. Tend to silence brain circuits. |
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Term
| GABA(b) receptor general location (pre or post synaptic), and where it has its eff ct |
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Definition
| GABA(b) is often located on the pre-synaptic cell. GABA is released frmo a third neuron, and this, through G-protein coupling, will decrease the probability of vessicle release in the pre-synaptic cell |
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Term
| heterosynaptic facilitation..what is it, what NT does it utilize in Aplysia, and what effect does this have on ion channels? |
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Definition
| Process in which a synapse is strengthened by the input of other facilitating interneruons. It happens, specifically in Aplysia, when 5-HT FROM THE FACILITATING INTERNERUON activates a cascade of second messengers that leads to the closing of K+ channels, lengthening the duration of action potentials. |
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Definition
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Definition
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Term
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Definition
| GABA(b) agonist. Enhances GABA's effect. |
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Term
| glutamate and basic receptors |
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Definition
| Brain's major excitatory transmitter. Basic ionotropic receptors are AMPA and NMDA. |
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Term
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Definition
| "Neurons that fire together, wire together." Because of the mechanism of LTP involving silent synapses, two neurons that firing at the same time can lead to a strengthening in the neuron's synapses |
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Definition
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Term
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Definition
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Term
| AMPA - effect of glutamate? Ion conductances? What is the depolarization it causes like? |
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Definition
| AMPA is a simple EPSP channel with a mixed cation conductance to K+ and Na+. Its release shows a quicker depolarization than NMDA. |
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Term
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Definition
| NMDA is blocked by Mg++ when it is hyperpolarized, and thus its channels, which allow Ca++, Na+, and K+ to pass, are closed. To open the NMDA channel, the cell must be A) Depolarized and B) Bound to both glycine and glutamate. |
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Term
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Definition
| Series of events in which damage occurs, leading to seizures. Increasing the concentration of glutamate, NMDA is activated, increasing intracellular calcium. Can have maintained periods of elevated Ca++ concentrations, triggering neuronal death. Because this is increasing the rate that nearby neurons fire as well, can cause lesions. |
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Term
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Definition
| A single, quick shock at high frequency. |
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Term
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Definition
| Capture synaptic potentials in a large population of cells. Larger electrode. |
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Term
| Area of the brain commonly sliced when looking at LTP |
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Definition
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Term
| Importance of Calcium in LTP |
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Definition
| Calcium is important in LTP. It is first allowed in with an active NMDA receptor. It phosphoryllates CAM-Kinase-2, which allows the silent AMPA receptors to surface on the membrane, thus increasing future responses to depolarization... |
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Term
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Definition
| Need selectivity, or all neurons will just get increasing strong. Slowly, over time, overactive synapses will degrade in their absolute strength, and underactive synapses can be upregulated. Overall, though, the synapses maintain their overall relative strength. |
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Term
| What does synaptic scaling suggest about a cell's activity level? |
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Definition
| It suggests that cells may have encoded target activity levels... |
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Term
| Serotonin - basic functions (on behavioral level) |
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Definition
| Affects sleep, mood, learning, etc. |
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Term
| Gill-withdrawal reflex in Aplysia (a mollusk) |
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Definition
| Extraordinarily simple form of learning. Poke the gill, mollusk withdraws it. Hit its siphon, and it withdraws the siphon and its gill. Hit the tail, it withdraws the tail and its gill. |
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Term
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Definition
| Decrease in response to a repeated stimulus |
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Term
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Definition
| Enhancement of response to repeated stimulus |
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Term
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Definition
| respond to internal or external stimulus. Bring info into the system. |
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Definition
| innervate muscles, produce movement. |
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Term
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Definition
| All neurons in between sensory and motor neurons |
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Term
| Using dyes to discover which neurons sensory, etc. |
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Definition
| You put dye into a cell and see which cells are stained after causing cells to fire an AP (by poking). These are candidate neurons. |
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Term
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Definition
| When there is no intervening neuron between a motor and sensory neuron |
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Term
| How do you tell whether or not there is an interneuron between sensory and motor neurons experimentally? |
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Definition
| Look for a short, consistent latency. Fire the cell repeatedly, and look for a fixed delay between APs. |
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Term
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Definition
| Made of opsin and retinal (vitamin A). Retinal starts the phototransduction cascade |
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Term
| Phototransduction cascade |
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Definition
| Photon of light hits rhodopsin. 11-cis retinal changes into 11-trans retinal, which activates transducin, a g-protein downstream. Transducin then activates cGMP phosphodiesterase. This turns cGMP into 5-GMP, which closes the cGMP gated sodium channel. This ultimately hyperpolarizes the cell. |
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Term
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Definition
| Binds to phosphoryllated rhodopsin kinase tightly, blocking the transducin effect. |
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Term
| Possible deficiencies in color vision |
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Definition
Protanopia - red
deteropia - green
tetanopia - blue (rare) |
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Term
| Why does serotonin broaden spikes? |
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Definition
| As discovered in a patch-clamp experiment, serotonin activates a second messenger system that leads to a large decrease in K+ conductance (the delayed rectifier), which will lengthen the duration of spikes. |
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Term
| In short term sensitization, there are multiple second messenger pathways possible. Name the two pathways given in the example in class/their ultimate effect on the cell? |
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Definition
| There were 2 second messenger systems given in class. One receptor receives 5-HT from the facilitating interneuron and activates a cascade starting with the activation of guanyl cyclase, producing cAMP, which activates PKA, which ultimately decreases delayed rectifier potassium conductance, prolonging the spikes. Also, another pathway activates DAG, which activates PKC, which also decreases potassium conductance, having the same effect (the S current). Both of these cascades increase the readily releasable pool of vessicles. Ultimately the lengthened spikes allow more Ca++ to enter the cell, and allow more vessicles of transmitter to be released after a spike. |
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Term
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Definition
| Higher amplitude synaptic potentials providing STABLE SENSITIZATION. Generally involve some sort of protein synthesis for permanent change. |
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Term
| How many applications of serotonin required for short term sensitization in Aplysia? Long term? |
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Definition
| A single application of serotonin can cause short term sensitization in Aplysia, while long term effects require at least 5 applications, spacedo ut over time. Repeated training. |
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Term
| What activity is increased by repeated applications of serotonin in long term sensitization? The cascade sequence after that is? |
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Definition
| PKA and PKC, which go into the nucleus and increase the phosphoryllation of CREB1. This ultimately increases transcription in many genes and downregulates the effects of NCAMs, allowing a restructuring of the dendritic tree. Ultimately, this means that there can be more synaptic terminals created. |
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Term
| How does a cell demonstrate short term sensitization? |
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Definition
| It increases the amount of transmitter released |
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Term
| How does a cell demonstrate intermediate term sensitization? |
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Definition
| With the help of 5-HT, begins to mobilize vessicles into those synapses with smaller releasing sites. |
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Term
| How does a cell demonstrate long term sensitization? |
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Definition
| The cell will, through the cascade that suppresses NCAMs, sprout new synapses (after transcription) to, in the long term, increase then number of synaptic sites... |
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Term
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Definition
| The place in the environment in which a neuron is best activated (either excitatory or inhibitory) |
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Term
| rate coding in sensory neurons |
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Definition
| The firing rate of a neuron is sufficient to distinguish stimulus intensity |
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Term
| temporal coding in neurons |
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Definition
| Frequency coding in the PATTERNS of APs can contain information about stimulus intensity |
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Term
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Definition
| The idea that a photoreceptor in the eye inhibits neighboring photoreceptors when activated. This allows for constrast enhancement. |
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Term
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Definition
| In the presence of Ca++, can bind to the SNARE complex allowing the vessicle fusion reason to proceed. |
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Definition
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Term
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Definition
| Excitatory because ECl is higher |
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Term
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Definition
| Removes Ach from alpha-bungaro toxin |
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