Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

19 Cards in this Set

  • Front
  • Back
blockers of the AchR?
curare and alpha bungarotoxin
can AchR channels inactivate?
when Ach is present for a long time, they may desensitize
what is the ion selectivity for the AchR?
it is a mixed cation channel. Lets Na and K through. has a reversal potential around 0. Also a small amount of Ca, which is important for development.
what are some characteristics that allow NMJ transmission to be hi-fidelity?
-large amounts of Ach released into the cleft promotes binding

-AchR channels open very fast

-Ach is degraded or diffused quickly

-AchR recovers quickly w/o desensitization

-AchR has low affinity for substrate so that as soon as the Ach has been removed from the synapse (1.AchE 2.diffusion.), the AchR:Ach will dissociate and the channel will close and go back to resting state
what is the difference between an AP and an EPP?
an AP is regenerative.
an EPP decays with distance b/c current leaks out.
what is the quantal hypothesis
the epp is the summation of many tiny units that are identical in size. these miniature depolarizations are due to one vesicle of Ach being released and the resulting depolarization triggered by it binding to AcR.
what is quantal content?
quantal content is the number of vesicles released with each AP.

at each NMJ, a normal epp is 200 quanta/vesicles
describe process of vesicle cycling
Docking - vesicle is tethered to presynaptic membrane
Priming - vesicle undergoes biochemical changes to ready it for fusion. All it needs now is Ca.
Fusion - Ca causes the vessels to fuse to membrane
Endocytosis - keeps the bouton from getting bigger and bigger
Fusion w/ endosome
Filling with NT
what causes the delay b/t the AP at the NMJ and the release of NT?
the majority of the delay is caued by the Ca channels being slow to open. they open more slowly than Na channels.
why are presynaptic microdomains important for synaptic transmission?
the Ca only gets high near the Ca channel (Ca hot spot)
the Ca channels are located very near the synaptotagmin (Ca sensor) at an active zone.
What is synaptotagmin's affinity for Ca?
synaptotagmin has a low affinity for Ca, but it is located very close to the Ca channel where the local Ca is very high momentarily. everything is tethered together at the active zones.
what are some differences and similarities b/t central synapses and NMJ?
an NMJ has Ca channels and tethered vesicles located at active zones directly across from the AchR located at the mouth of a junctional fold. when an AP reaches the axonal bouton, there is much more Ach release and AchR binding than is needed to create an AP. this is the saftey zone. lots of factors make this hi-fi transmission.

Central synapse is like a single active zone. One neuron may have 10000 dendrites receiving signals from many axons. temporal and spatial summation depolarize the cell to fire it.

different needs. different organization.
what is the primary way to remove NT in the CNS and at the NMJ
NMJ: 1. AchE 2. lateral diffusion

CNS: lateral diffusion mainly
why is AchE inhibitor not a totally effective treatment for MG?
AchE is taken care of, but lateral diffusion still decreases Ach and terminates signal. junctional folds are shallower and cant "store" as much Ach.
axo- somatic, dendritic, and axonic; dendrodendritic synapes

what do each of these usually do?
axosomatic - usually inhibitory
axodendritic - usually excitatory
axoaxonic - can have facilitory or depressant effects on transmission
dendrodendritic - reciprocal excitation in the olfactory bulb
what is shunting inhibition?
shunting inhibition is how an IPSP can stop an EPSP from causing an AP in a post synaptic cell. the IPSP opens chloride channels, and the conductance is MASSIVE. because the conductance is so high, this essentially clamps the cell's membrane potential at the nernst/eq'm/reversal potential of chloride.
when could an IPSP be depolarizing?
when the cell's RMP is less than Cl's equilibrium potential. Cl's equilibrium potential may vary.
what 2 kinds of summation are important in determining if an EPSP can trigger an AP?
spatial and temporal summation
how do glia prevent excitotoxicity?
when CNS neurons fire, the main way of terminating the signal is lateral diffusion. if the extracellular glutamate rises too much, this can cause cytotoxicity. Glia take glutamate up and convert it to glutamine.