Term
| Neuron’s resting potential _______. |
|
Definition
|
|
Term
| Depolarization is caused by ______ postsynaptic potentials. |
|
Definition
|
|
Term
| Hyperpolarization is caused by ________ postsynaptic potentials. |
|
Definition
|
|
Term
| Synapses are located on ________ or ________. |
|
Definition
dendritic spines
the cell body |
|
|
Term
| ________ is caused by excitatory postsynaptic potentials. |
|
Definition
|
|
Term
| ________ is caused by inhibitory postsynaptic potentials. |
|
Definition
| Hyperpolarization (Inhibiting the cell) |
|
|
Term
| Excitatory Post Synaptic Potential _____ the chances of a neuron firing. |
|
Definition
|
|
Term
| Inhibitory Post Synaptic Potential _____ the chances of a neuron firing. |
|
Definition
|
|
Term
| what is Decremental Conduction? |
|
Definition
| as you move along the neuron, the strength of the signal fades |
|
|
Term
| What is Spatial summation? |
|
Definition
| when more than one cell fires together onto a cell, the post synaptic potentials add together (intergration) |
|
|
Term
| What is Temporal summation? |
|
Definition
| when a cell fires in rapid succession onto a cell, the post synaptic potentials add together (intergration) |
|
|
Term
| when summation reaches ________ the neuron fires |
|
Definition
| the threshold of excitation |
|
|
Term
Action potential: a massive rapid (1 millisecond) reversal
of the membrane potential from _____ to _____. |
|
Definition
|
|
Term
| In the axon’s membrane adjacent to the ________. |
|
Definition
|
|
Term
| what is the the threshold of excitation? |
|
Definition
|
|
Term
| What are the steps of an action potential? |
|
Definition
1)Na+ channels open causing a Massive influx of Na+ ions
4)The cell membrane starts depolarizing which opens K+
channels (“voltage gated”), and K+ ions exit the cell following their concentration gradient
5) Full depolarization of the cell membrane (+50 mV) and Na+ channels close
6) K+ ions still exit the cell because of electrostatic
pressure (inside of cell has become positive)
7) cell membrane starts REpolarizing and K+ channels close gradually
8) There is Temporary hyperpolarization followed by a Refractory period |
|
|
Term
During Depolarization: ____ channels open causing a massive influx of ___ ions. The cell membrane starts
depolarizing. Depolarization opens ___ channels (“voltage gated”). ____ ions exit the cell following their concentration gradient. |
|
Definition
Na+ channels open, Na+
K+, K+ |
|
|
Term
| What is the difference between Absolute Refractory Period and Relative Refractory Period? |
|
Definition
Absolute Refractory Period: the interval during which a second action potential absolutely cannot be initiated, no matter how large a stimulus is applied
Relative Refractory Period: the interval immediately following during which initiation of a second action potential is inhibited but not impossible |
|
|
Term
Why can the eye can perceive high or low intensity
light stimulations? |
|
Definition
| Due to the refractory period. With a weak stimulation, the neuron will have to wait until the refractory period is over, but with a strong stimulation, the refractory period can be shortened, and we sense this difference in firing frequency. |
|
|
Term
Why can a muscle can be contracted at different
strengths? |
|
Definition
| Due to the refractory period. With a weak stimulation, the neuron will have to wait until the refractory period is over, but with a strong stimulation, the refractory period can be shortened, and we sense this difference in firing frequency. |
|
|
Term
Why can the secretion from a gland can be stimulated
at high or low levels? |
|
Definition
| Due to the refractory period. With a weak stimulation, the neuron will have to wait until the refractory period is over, but with a strong stimulation, the refractory period can be shortened, and we sense this difference in firing frequency. |
|
|
Term
| For a high intensity stimulus, the firing rate set by _____ refractory period. |
|
Definition
|
|
Term
| For a _____ intensity stimulus, the firing rate set by relative refractory period. |
|
Definition
|
|
Term
Action potentials _____ travel backwards within the
axon under natural conditions. |
|
Definition
|
|
Term
| What is Orthodromic conduction: |
|
Definition
| An action potential travelling in a normal direction, from axon hillock towards axon terminal. |
|
|
Term
| What is Antidromic conduction: |
|
Definition
| An action potential travelling in the opposite direction, from axon terminal towards axon hillock. |
|
|
Term
| ________ happen close to the synapse, are very fast, are decremental, and are passive. |
|
Definition
|
|
Term
| ________ happen along the axon, are slower, are nondecremental, and are active. |
|
Definition
|
|
Term
What is the difference between Post Synaptic Potentials
and Action Potentials. |
|
Definition
PSP happen close to the synapse, are very fast, are decremental, and are passive.
AP happen along the axon, are slower, are nondecremental, and are active. |
|
|
Term
| What part of an action potential is active? (And what part is passive? |
|
Definition
opening the Na+ (sodium) channels is active
when the Na+ enter the cell it is passive |
|
|
Term
| What is Saltatory Conduction? |
|
Definition
| conduction with a myelin sheath, which is fast! The Action potential is regenerated at the nodes of ranvier, and inbetween the signal degrades under the myelin sheath similar to EPSP. |
|
|
Term
| Why does myelin make the signal travel faster. |
|
Definition
In the myelinated apart of the axon, the signal travels as an EPSP, which is very fast! And only has to do AP in the nodes of ranvier, just to keep the signal going so it doesn't degrade.
In a non-myelinated axon the signal travels only by AP, which are all very slow. |
|
|
Term
| Why do cats have faster AP than cats? |
|
Definition
| Their large axons conduct very quickly. |
|
|
Term
| What is Synaptic transmission? |
|
Definition
| transmission of signal from one neuron to another? |
|
|
Term
What is the difference between
Axodendritic Synapses
Axosomatic Synapses
Dendrodendritic Synapses
Axoaxonal Synapses |
|
Definition
Axodendritic Synapses: Axon - Dendrites
Axosomatic Synapses: Axon – Cell body (soma)
Dendrodendritic Synapses: Dendrite - Dendrite
Axoaxonal Synapses: Axon - Axon |
|
|
Term
| Electrical synapses are ____ than chemical synapses, but they are only _____. |
|
Definition
|
|
Term
Which would be more likely to have more electrical synapse?
crayfish
mammal |
|
Definition
|
|
Term
|
Definition
| A type of electrical synapse made of 6 connexins making a connexon and 2 connexons make 1 gap junction. |
|
|
Term
|
Definition
| When neurons can synthesize and release different neurotransmitters. |
|
|
Term
| _______ molecules usually travel passively through the axon along a concentration gradient. |
|
Definition
|
|
Term
| Bigger peptides/proteins are usually packaged in the _____ and then travel ____ by ____. This process is very slow, about 40 cm/day. |
|
Definition
soma
actively by axoplasmatic transport |
|
|
Term
What is the difference between
Directed Synapses and Non Directed Synapses |
|
Definition
Directed Synapses: goes across a cleft
Non Directed Synapses: diffuses in that general area |
|
|
Term
When the action potential reaches the synaptic terminal,
________ channels open. |
|
Definition
| Voltage-activated Calcium (Ca2+) |
|
|
Term
| Presynaptic Vesicles fuse (dock) with the _______ and release their neurotransmitter contents in the ______. |
|
Definition
cell membrane
synaptic cleft |
|
|
Term
| what is the difference between an agonist and an antagonist? |
|
Definition
Agonist: a drug that facilitates the effects of a particular neurotransmitter
Antagonist: a drug that inhibits the effects of a neurotransmitter : |
|
|
Term
| What is the difference between competitive binding and non-competitive binding? |
|
Definition
Competitive Binding
Noncompetitive Binding |
|
|
Term
| In mice with NR2B overexpression, (MDA) what happend |
|
Definition
the mice have enhanced context and cue memory
both NR1 and NR2B are important in learning and memory |
|
|
Term
| What is Long-Term Potentiation (LTP)? |
|
Definition
An enduring change in communication between pre and post synaptic cells in response to salient stimulation
(including behavioural) |
|
|
Term
GABA is an _____, and ______ neurotransmitter.
(excitation/inhibition, type) |
|
Definition
|
|
Term
| GABA is synthesized from _______. |
|
Definition
|
|
Term
| What are the 3 GABA receptors? Which is the most common? |
|
Definition
GABA-A: ionotropic (Cl-) (most common)
GABA-B: metabotropic
(less common)
GABA-C : ionotropic (Cl-) |
|
|
Term
| what are allosteric sites? |
|
Definition
| GABA cannot bind here, but they modify the action of GABA |
|
|
Term
________ such as: (valium, librium). Are anxiolytic; muscle
relaxing; anti-convulsant; impair learning and memory.
(modulator of GABA) |
|
Definition
| Benzodiazepines (modulator of GABA) |
|
|
Term
______ are calming (low doses). Used for anesthesia (in higher
doses); impair learning and memory.
(modulator of GABA) |
|
Definition
| Barbiturates (modulator of GABA) |
|
|
Term
______, e.g. progesterone and its metabolites are calming.
(modulator of GABA) |
|
Definition
| Steroids (modulator of GABA) |
|
|
Term
| Which modulator of GABA is a poison found in an East Indian shrub? It inhibits GABAA receptors (indirect antagonist). At high doses it causes ______. |
|
Definition
|
|
Term
| Which sites does Alcohol regulates GABA-A function at? |
|
Definition
calming and relaxing.
-at the benzodiazepine site
-at the Barbiturate site |
|
|
Term
| how are MONOAMINE NEUROTRANSMITTERS synthesized? |
|
Definition
For each: one-step synthesis from one amino acid
They all begin at Tyrosine, and then depending on the enzyme they follow this chain at stop at one point
-L-DOPA
-Dopamine
-Norepinephrine
-Epinephrine
Localized synthesis (brain stem nuclei) by widespread function |
|
|
Term
Dopamine is synthesized in the ______ and goes to the ____.
It is also synthesized in the ______ and goes to the ____ and _____. |
|
Definition
Substantia nigra > striatum
and Ventral Tegmental Area > Limbic System and Prefrontal cortex |
|
|
Term
| Degeneration of dopamine causes _____. It is treated with ____. |
|
Definition
Parkinson’s Disease
You cannot use dopamine, it doesn't cross the BBB. L-Dopa is used instead. As long as there are still neurons there it can be used. L-Dopa boosts ALL dopaminergenic neurons not just dopamine, so inhibitory feedback is triggered. So lots of side effects. |
|
|
Term
| What are the Two subfamilies of 5 dopamine receptors? |
|
Definition
D1–like: D1 and D5
D2–like: D2, D3 and D4 |
|
|
Term
| What many functions is Dopamine involved in? |
|
Definition
Movement (NS)
Attention
Learning
(food, sex, drugs of abuse)
major component of the reward system: mesolimbic pathway (nAcc) (reinforcements like food, sex, drugs) |
|
|
Term
| What is the vole (dopamine) example? |
|
Definition
-Voles develop a monogamous bond with their partner
-Bonding is sustained by the reward system effects on dopamine |
|
|
Term
| ______ are agonist dopaminergenic drugs. Used to treat Disorders of excessive sleep. |
|
Definition
|
|
Term
| ______ are D2 receptor antagonists dopaminergenic drugs used to treat schizophrenia. Side effects on the _____. |
|
Definition
Antischizophrenic (Antipsychotic) drugs
motor side effects: cause too much activation, facial tics, jerks |
|
|
Term
| _____ is Synthesized mainly in the pons (metencephalon), specifically in the ______. It is released by _____. |
|
Definition
Norepinephrine
Locus ceruleus
diffusion |
|
|
Term
| what does Norepinephrine effect |
|
Definition
| arousal, attention, attention, learning, and memory |
|
|
Term
| _______ is synthesized In the medulla of the adrenal glands in the kidneys. In the Periphery, it acts in the nervous system. In the CNS, it has limited role as an ______ molecule. |
|
Definition
adreneline
autonomic
neurotransmitter/neuroactive molecule |
|
|
Term
| What are the Adrenergic Receptors? The respond to ____. |
|
Definition
α1 – α2 – β1 – β2
Responses to arousing, activating, stressful events. |
|
|
Term
Epinephrine is mostly in the _____
Norepinephrine is mostly in the _____ |
|
Definition
Epinephrine mostly in the periphery
Norepinephrine mostly in the CNS |
|
|
Term
| ______ receptors are implicated in ADHD. A common treatment for ADHD is _____. |
|
Definition
|
|
Term
| what are Monoamine oxidase inhibitors |
|
Definition
| formerly used to treat depression; side effects |
|
|
Term
| _____ (e.g. propanolol): used for anxiety disorders (e.g., GAD); reduce peripheral aspects of anxiety (sympathetic activation), not anxiety per se. |
|
Definition
|
|
Term
|
Definition
increases activity of both Dopamine and Norepinephrine.
It blocks their reuptake, but the synapses remain active.
So dopamine accumulates and has analgesic properties. |
|
|
Term
| What is COCAINE PSYCHOSIS? |
|
Definition
Caused by overuse of cocaine. Excitability, anxiety, talkativeness, increased pulse rate and blood pressure, dilation of pupils, faster breathing,temperature, sweating, loss of appetite, insomnia.
Bizarre, erratic, sometimes violent behavior and paranoid psychosis that disappears if discontinued. Sometimes misdiagnosed as Paranoid Schizophrenia |
|
|
Term
| Serotonin is synthesized from _____, in the ______. From the three areas of this, where does it go? |
|
Definition
tryptophan
Serotonin
midbrain, pons and medulla: Mainly in neurons of the raphe nuclei
Dorsal raphe goes to the basal ganglia/cerebellum, and cerebral cortex (motor control)
Median raphe goes to the Cerebral cortex (higher cognitive functions) |
|
|
Term
| ______ is a serotonin reuptake inhibitor. Active component of Prozac, used to treat: ___, ____, and ____. |
|
Definition
seretonin
Depression Some forms of Anxiety Disorders and Obsessive Compulsive Disorder |
|
|
Term
| _____ is a reuptake inhibitor AND stimulates release. It used as a |
|
Definition
Fenfluramine:
Appetite suppressant, formerly used to treat obesity
discontinued because it caused heart disease |
|
|
Term
| Lorcaserin: selective 5-HT receptor agonist used for: |
|
Definition
| Satiety enhancer. Approved by the FDA in June 2012 to treat obesity |
|
|
Term
| _______ is associated with Cholinergic neurons. It is released at Neuromuscular junctions when muscles contract. It is involved with Brain functions: regulation of sleep, learning, memory. |
|
Definition
|
|
Term
| Acetylcholine is produced in _______. |
|
Definition
| Brain stem nuclei – in pons and midbrain |
|
|
Term
| _______ is an an anaerobic bacterium that blocks the absorption of acetylcholine causing paralysis. It is food-borne, and can be acquired from contact with a wound, or inhalation. |
|
Definition
Botulinum Toxin (Botox)
paralysis |
|
|
Term
| Botox causes _____ by blocking the release of Ach. How does recovery occur? |
|
Definition
| New motor axons can grow and form new synapses, but is not always complete |
|
|
Term
| What are the Therapeutic uses of Botox? |
|
Definition
-used to treat blepharospasm (people who cannot open their eyelids properly) by stopping the muscles of the eyelid
-used to treat migraines caused by muscle spasms
-used to relax skin and ease the appearance of wrinkles, but they can interfere with facial expressions |
|
|
Term
| Black Widow Spider Venom: it stimulates the release of _____, causing _____. |
|
Definition
Ach
Muscle spasms/convulsions. |
|
|
Term
| What are the 2 ach receptors? What kind of receptor are they? |
|
Definition
Muscarinic receptors: metabotropic
Nicotinic receptors: ionotropic |
|
|
Term
| The extract of the belladonna plant is called ______. Which receptor does it interact with? |
|
Definition
Atropine:
Competitive muscarinic ACh
receptor antagonist (blocker) |
|
|
Term
| What is Scopolamine? What is the example for it? |
|
Definition
competitive muscarinic receptor antagonist (Ach) prevents binding of ACh
mice injected with Scopolamine show a very low discrimination between old objects and new objects. |
|
|
Term
______ is an extract of certain woody vines in South America.
It works by causing paralysis through __________. It acts on the _______ receptors. |
|
Definition
Curare
respiratory constriction
Nicotinic ACh receptor antagonist (blocker) |
|
|
Term
ACh and agonists (e.g.,_______) acting on nicotinic
receptors in brain and can ______ working memory and
attention. It may have implications for the treatment of ____ and _____. |
|
Definition
nicotine
enhance
Schizophrenia/ADHD |
|
|
Term
| SOLUBLE GAS NEUROTRANSMITTERS are Very _____ lasting – very ____ active. They have _____trograde transmission of cellular signals. |
|
Definition
|
|
Term
| ______ is synthesized in neurons from arginine. Acts on ____ messengers of several pathways: (e.g. vasodilation (viagra), pain, learning and memory?; etc.) |
|
Definition
|
|
Term
| Carbon Monoxide (CO): produced is ____ neurons. Functions similar to NO, but still not well understood. |
|
Definition
|
|
Term
| PEPTIDE NEUROTRANSMITTERS are short chains of amino acids. What are the 5 kinds? |
|
Definition
Pituitary peptides
Hypothalamic peptides
Brain-gut peptides: made by brain OR gut
Opioid peptides
Miscellaneous peptides |
|
|
Term
Peptides are generally Produced and packaged in vesicles in the _____. Active axonal transport, and Released by _____ by the terminal button. Some are neurotransmitters
Others are neuromodulators. |
|
Definition
|
|
Term
| What are the 3 endogenous opioid Peptides? What do they effect? WHere are the receptors? |
|
Definition
beta-endorphin, enkephalins, dynorphin
pain perception/analgesia
Periaqueductal gray, hypothalamus, other brain areas |
|
|
Term
| what is the difference between opioids and opiates? |
|
Definition
opioids- made by the body
opiates- made externally and act on opioid receptors |
|
|
Term
Which Opioid is an antagonist/agonist?
Naloxone
Morphine |
|
Definition
Morphine: opioid agonist
Naloxone: opioid antagonist |
|
|
Term
| OXYTOCIN is Synthesized in the ______. It is Released in the ______ through the _______. It activates the receptor _____ in the ______. |
|
Definition
Hypothalamus
blood stream
pituitary gland
OTR
Brain |
|
|
Term
| _______ regulates labor/parturition, lactation/nursing, maternal behavior, social affiliative behavior including pair bond, maternal bond, social recognition. |
|
Definition
|
|
Term
| What 2 studies give evidence for The Oxytocin system and Social Recognition in mice? |
|
Definition
[1] Oxytocin global knockout in mice, they don't produce oxytocin, but have normal receptors
-these mice investigate a familiar mouse again and again, and do not change between old and new mouse
[2] Antisense DNA against the gene for the oxytocin receptor, Stereotaxic injection in the brain of “normal” mice, and had no receptor
-these mice also do not habituate to an old mouse and show more interest in a new mouse, unlike scrambled DNA group or blank group |
|
|
Term
What are the two Lipids: cannabinoids NEUROTRANSMITTERS?
What do they do? |
|
Definition
exogenous: cannabis, in marijuana
endogenous: anandamide
reduce: pain, memory
increase: sleep, feeding, (it’s a relaxing drug) |
|
|
Term
| The Nucleoside adenosine ______ (inhibitory / excitatory) neurotransmitter. It is produced by _____. |
|
Definition
|
|
Term
estrogens, testosterone, progesterone, cortisol and several metabolites are examples of ________. They control sex-related physiologic functions
stress physiologic responses
sex-related behaviour
stress/anxiety related behaviour
individual recognition
aggression, learning |
|
Definition
|
|
Term
Steroid hormones
Nuclear receptors / cytosolic receptors have ______ lasting _____ effects
Membrane receptors also exist _______ lasting _____ effects |
|
Definition
long, genomic
rapid, nongenomic |
|
|
