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37 Cards in this Set
- Front
- Back
What NT's precipitate an EPSP?
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Glutamine and Acteylcholine
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What NT's are involved in IPSP?
What kind of channels do these use? |
GABA and Glycine -
LIGAND GATED ION CHANNELS. |
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What effect does increase in permeability to Cl- have on synaptic transmission?
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This is INHIBITORY. GABA and Glycine are used in this inhibitory pathway.
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Which kinds of presynaptic contacts are inhibitory?
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AXOSOMATIC and AXOAXONIC are usually inhibitory.
Axodendritic with contact at the shaft is inhibitory as well. |
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Which kinds of presynaptic contacts are excitatory?
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AXODENDRITIC - axon to dendrite end (not shaft) are excitatory
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How many EPSP's does it take to get to an action potential?
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These are GRADED...so more than one.
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What is spatial summation?
When is this most effective? |
EPSP's arising simultaneously at multiple synapses on the dendrites or soma.
Spatial summation is most effective when LENGTH CONSTANT IS LONG. |
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What is temporal summation?
When is it most effective? |
When a single NT is released at a single synapse frequently enough to get electrical summation of individual EPSP's.
Temporal summation is most effective when TIME CONSTANT IS LARGE. |
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When there is a large time constant, what kind of summation is most effective?
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Temporal summation - the one with ONE
synapse getting fired on many times in a row. |
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When there is a long length constant - which kind of summation is most effective?
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Spatial summation.
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In the CNS, is there a low or high probability that an AP will evoke the release of a vesicle?
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Probability is low in the CNS.
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What opens Ca+ channels?
What happens when they are open? |
Action potential opens Ca+
Entry of Ca+ into the cell will release NT into synapse. |
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What has bigger impact on amount of neurotransmitter release - the gating properties of Ca+ or the duration of the AP?
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The duration of the AP has the biggest effect on amount of NT released.
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What are three examples of peptide NT's?
Are there more kinds of small-molecule neurotransmitters or peptide NT's? |
ex) substance P, enkephalin and LHRH
there are many more kinds of peptide NT's than small molecules like Ach/Glu |
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What is classic presynaptic inhibition?
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Usually axoaxonic inhibition.
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What is this:
T=RmCm |
Time constant = loss of current through leak channels X capacitance
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Are time constant and length constant affected by voltage-gated Na+ channels?
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NO these are passive properties.
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Why does it makes sense that spatial summation is most effective when length constant is long?
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When length constant is long - the decrement over the length of the axon is LOW - so over that span - a greater number of spatially separated EPSP's can sum.
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Where do you find peptide neurotransmitters vs. small-molecule NT's?
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small-molecule NT's are found localized to active zones.
peptide NT's (called dense-core vesicles) are distributed around the periphery of the synaptic terminal. |
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What is responsible for termination of NT action in the CNS?
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Termination occurs via reuptake of NT into synaptic terminal by transporters SPECIFIC for the NT and diffusion.
They are co-transported with Na+ who's concentration gradient provides the energy. |
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what is a motor endplate?
What is the junctional cleft? |
The area on the muscle fiber that is directly under the axon terminal.
The space between these two regions. |
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Where are active zones found in the NMJ?
Where is a junctional fold? |
on presynaptic structures
a fold in the motor endplate |
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How does an EPP arise?
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Ach is released into the junctional cleft and diffuses to the motor end plate.
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What kind of ion channel is an Ach receptor?
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Ach receptor is a LIGAND GATED ion channel.
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What surrounds the muscle fiber and axon terminal to maintain the fold structures?
What enz does this space contain? |
Lamina Basliaris = surrounds these tissues and contains acetylcholinesterase
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Where does inhibition occur in the CNS or PNS?
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ALWAYS CNS - there are NO INHIBITORY neurons in the PNS. PNS contains all excitatory motor neurons.
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Are EPP's or EPSP's graded?
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EPSP's are graded. EPP's always result in an AP in muscle.
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How do EPP's terminate?
How is this different than EPSPs? |
EPP's terminate bc acetylcholinesterase cleaves.
Both EPSPs and EPPs use diffusion...but only EPPs use acetylcholinesterase. |
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What guarantees EPP at NMJ?
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The amount of Ach released is more than necessary
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What is an MEPP?
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When vesicles randomly fuse with the internal surface of the axon membrane (not requiring Ca+) - each vesicle that fuses with the membrane releases a single quantam of ACh - gives rise to MINIATURE ENDPLATE POTENTIAL.
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The acetylcholine receptor is made of what?
What is desensitization of ACh receptors? |
Integral membrane proteins.
Desensitization = the net depolarizing current through the channel gradually decreases despite continued binding of ACh by the receptors. |
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Why are the ACh-sensitive ion channels in the endplate region not affected by voltage changes?
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ACh-sensitive ion channels are LIGAND GATED. The motor endplate does not generate an AP - but it does depolarize the muscle membrane to threshold so an AP will fire next to it.
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What is gallamine?
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Gallamine is a competitive neuromuscular blocking agent - it inhibits Ach binding resulting in muscle paralysis.
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Are AP's generated with competitive neuromuscular inhibitors?
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No AP. Just paralysis.
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Does succinylcholine cause an AP before blocking ACh receptors?
How do these work? |
Yes (unless administered slowly which takes advantage of desensitization).
Much slower to dissociate from receptor so voltage gated Na+ inactivate in muscles = tissue now REFRACTORY. |
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What is nerve gas?
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blocks acetylcholinesterase = increase ACh in junction = paralysis by depolarization block and desensitization.
LETHAL. |
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What is myasthenia gravis?
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degenerative muscle weakness caused by antibodies that attack ACh receptors.
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