Term
| how many synapses per neuron |
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Definition
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Term
| how many ACh molecules in a single vesicle in a NM junction? |
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Definition
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Term
| a single action potentio at the NM junciton will release ___ vesicles in ___ ms |
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Definition
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Term
| it takes ACh ____ms to traverse the ___ nm synaptic cleft |
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Definition
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Term
| what type of cholinergic receptors are at the NM junction? |
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Definition
| nicotinic, they are at a very high density (10,000/ 1um^2) |
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Term
| AChR is a ____ ____ channel that depolarizes the muscle cell ____ mV in< _____ ms |
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Definition
| nonspecific; cation; 50-70; 0.1 |
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Term
| The time that an AP reaches the presynaptic cleft of a NM junction to the depolarization of the muscle is around ___ ms |
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Definition
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Term
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Definition
| neurexin (which binds synaptotagmin). latrotoxin prevents release of vesicles |
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Term
| Synaptobrevin is bound by which two toxins? |
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Definition
| botulinum toxin and tetanus toxin (both degrade synaptobrevin) |
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Term
| w-agatoxin, w-conotoxin and dihydropyridines |
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Definition
voltage dependent Ca++ channel blockers. w-agatoxin is spider venom, w-conotoxin is snail venom. They prevent synaptic release.
conotoxin is specific to N-type voltage dependent Ca++, which is implicated in pain fibers, so it can be used as an analgesic. |
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Term
| what does botulinum toxin do? |
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Definition
| blocks ACh release (synaptobrevin degradation). presynaptic |
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Term
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Definition
| postsynaptic ACh competitive antagonist. |
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Term
| alpha-bungarotoxin mechanism |
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Definition
| irreversibly binds to ACh: used to isolate ACh |
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Term
| Sarin & mustard gas mechanism: |
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Definition
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Term
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Definition
| AChase inhibitor. Used to treat myasthenia gravis |
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Term
| EPP are typically ____ mv, while EPSP/IPSP are ___mv, allowing for ____ |
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Definition
| 50-70 mv; 1 mv; summation |
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Term
| slow synaptic potentials are responsible for: |
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Definition
| releasing high MW neurotransmitters (neuropeptides) |
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Term
| how to neuropeptides and small molecule neurotransmitters get to the presynaptic terminal, respectfully? |
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Definition
neuropeptides are packaged in the cell body and transported down in vesicles: fast anterograde transport, 400 mm/day
proteins for making small molecules travel down the axon via slow axoplasmic flow. (1-2mm/day) |
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Term
| what are the 3 glutamate receptors? |
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Definition
NMDA, AMPA, Kainate
NMDA is important for learning and has a ton of agonists including ethanol, ketamine, PCP |
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Term
| GABA and Glycine receptors roles, respectively |
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Definition
GABA: Cl- channel, most fast IPSPs in brain
Glycine: Cl- channel, most fast IPSPs in spinal cord |
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Term
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Definition
| ethanol, barbiturates, benzodiazepine, |
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Term
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Definition
An enhancer of transmission
it crosses the blood-brain barrier and is metabolized into dopamine. This helps with the lower dopamine levels in Parkinson's disease. |
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Term
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Definition
an enhancer of transmission:
it increases the release of norepinephrine and dopamine. Acts as a stimulant |
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Term
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Definition
enhancer of transmission:
increases frequency of opening of GABA gated Cl- channels |
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Term
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Definition
enhancer of transmission
increases the time that GABA gated Cl- channels are open |
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Term
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Definition
enhancer of transmission
binds opioid-gated GPCRs causing analgesic effects |
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Term
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Definition
enhancer of transmission
fluoxetine (prozac) blocks the reuptake of serotonin |
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Term
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Definition
enhancer of transmission
blocks reuptake of dopamine and norepinephrine |
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Term
| pyridostigmine (mestinon) mechanism |
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Definition
enhancer of transmission
blocks AChase, used to treat myasthenia gravis |
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Term
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Definition
enhancer of transmission
blocks presynaptic adenosine receptors, preventing neurotransmitter release inhibition (blocks retrograde signaling) |
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Term
| vesimicol and reserpine mechanisms |
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Definition
depresses transmission:
block packaging of acetylcholine and amines (respectively) into vesicles. (interference with synthesis or packaging) |
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Term
| botulinum toxin mechanism |
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Definition
depresses neurotransmission
degrades synaptobrevin and prevents release of ACh |
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Term
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Definition
depresses transmission
degrades synaptobrevin and prevents glycine release: rigid paralysis |
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Term
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Definition
depresses transmission
blocks glycine-gated Cl- channels. Causes convulsions and other signs of hyperexcitability |
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Term
| Phenylcyclidine (PCP) mechanism |
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Definition
depresses transmission
blocks NMDA receptors |
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Term
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Definition
depressor of transmission
blocks skeletal muscle nicotinic receptors causing paralysis |
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Term
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Definition
depressor of transmission
blocks autonomic nicotinic receptors |
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Term
| Haloperidol (haldol) mecanism |
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Definition
depresses transmission
blocks dopamine GPCRs. acts as a antipsychotic |
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Term
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Definition
depresses transmission.
blocks muscarinic GPCR ACh receptors. causes autonomic changes
Atropine was used by cleopatra to dilate her pupils |
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Term
| in the spinal cord, ____ is the major excitatory NT and ____ is the major inhibitory one |
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Definition
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Term
| axons on dendrites are typically _____, on the soma are typically ____. Axons in the ____ are most potent |
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Definition
| excitatory; inhibitory; spike-initiation-zone |
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Term
| long time constant increases ____ summation, long length constant increases ___ summation |
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Definition
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Term
| heterosynaptic depression and facilitation are: |
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Definition
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Term
| renshaw cells are an example of what type of information processing? |
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Definition
| feedback inhibition: Ia afferents are depressed if they overstimulate renshaw cells |
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