6- synap phys 2 Flashcards

1
Q

What is mechanism that determines whether synapse is direct (fast) or indirect (slow)

examples of each

A

Fast = ionotropic (NT act directly on ion channel)

Slow = metabotropic (NT acts on GPCR and requires activ of 2nd messenger)

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2
Q

What is example of ionotropic and metabotropic mechanisms

A

ex = muscle fiber depol –> ACh bind nicotinic AChR –> open NSC channel –> Na+ enter –> muscle depol

ex = opening of K+ channel in heart
ACh bind muscarinic AChR –> activ GPCR –> gammaBeta released and diffuse to K+ channel –> open and K+ exits

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3
Q

What channel is opened in fast excitation? What is major NT involved?
What ions is permeable

A

major excitatory NT =glutamate and opens non-selective cation channel
permeable to Na and K

Na enter cell and depol

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4
Q

Define elctrical driving force

What is it the difference btwn

A

force to move ion across membrane (difference btwn voltage ion wants to be at (equilibrium) and actual membrane potential (Em))

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5
Q

Define reversal potential

A

Reversal potential = due to many NSC channels open –> membrane potential settle btwn ENa and Ek (~10 mV)

since greater than threshold –> therefore, excitatory and membrane depol

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6
Q

what kind of channel is opened during fast inhibition
main NT involved?

Which direction is the ion moving?

A

GABA
opens Cl channels in postsynap membrane

Cl- equilibrium potential more negative than threshold potential so Cl- movement does NOT CAUSE ACTION POTENTIAL

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7
Q

Why is inhibition more powerful than one might predict from size of an IPSP

A

b/c depends on relative permeabilities of ions

Small IPSP can reflect huge permeability change if ion’s equilibrium potential is close to resting membrane potential

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8
Q

Distinguish btwn temporal and spatial summation of postsynap potentials

A

When two diff presynap inputs synapse on a single neuron, potentails added to form larger potential since large amt of NT released

IF single input stim twice in succession, 2nd rise can start rising before previous AP has ended

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9
Q

Mechanism of synpatic transmission

A

1) AP arrives
2) open VG Ca2+ channel
3) Ca2+ bind synaptotagmin causing fusion of lipids of vesicles and surface membrane
4) open fusion pore to release NT (exocytosis)
5) NT bind receptors

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10
Q

Postsynaptic response depends on

A

nature of postsyn receptor

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11
Q

3 ways of removing NT

A

1) diffuse out of cleft
2) recycle by pump back to presyn terminal using Na coupled carrier molec
3) NT destroyed using extracellular degradative enzymes (ex = Ach)

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12
Q

How do you recycle the vesicle

A

1) vesicle membrane reinternalized (endocytosis) and filled with NT
2) NT synth locally and pump via Na coupled transporters into vesicle

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13
Q
Speed 
Effect 
Strength 
Transmitter 
Termination 

of NMJ vs CNS synapses

A

fast vs. (fast or slow)

excitatory vs (excit or inhib)

strong vs weak

Ach vs many others (Ach, glu, GABA, 5-HT, DA, Asp…)

diffusion/degradation by esterase (reuptake) vs. reuptake or diffusion (degradation)

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14
Q

difference btwn postsyn membrane in skeletal vs. neuron

A

skeletal = many folds to incr density of NT receptors

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15
Q

Motor unit define

NT in motor synapses with muscle

A

motor unit = axon + muscle fibers

NT = ACh

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16
Q

Ach receptor is what type of channel

A

ligand gated ion channel (binding of Ach stim open gate and influx of Na to depol)

17
Q

what type of channel is ACh

A

NSC (permeable to all cations)

18
Q

components of ACh receptor

A
4 subunits (2A, B, C, D) around pore 
each A binds one ACh and must bind simult
19
Q

how to clear Ca from synapse

A

2 channels

1) ATP driven
2) Na/Ca exchanger

20
Q

What happens if ECl is equal to resting membrane potential

A

IPSP amplitude = 0 but would still be inhibitory on EPSP

21
Q

What happens when the NT causes a decr in K+ ion permeability

A

depolarized bc excitatory synapse

22
Q

Describe presynaptic inhibiton

A

inhib nerve terminal synape on excitatory presynap terminals

–> inhib release GABA –> open Cl in presynap cell –> decr Ca2+ ch, less excitatory NT release

shuts off input to cell without affect cell’s resting membrane potential or synaptic effect of other input

23
Q

Suppose a single excitatory input was stimulated twice in succession. The first EPSP was 10 mV in amplitude, and lasted 20 msec. The second stimulus was given 50 msec after the first, and the EPSP was 15 mV. Was the larger size due to facilitation or summation or both?

A

facilitation, of course, because the first EPSP had completely decayed before the second stimulus was given

24
Q

suppose the second stimulus in the example above was given only 10 msec after the first, and the peak of the EPSP was 15 mV.

A

temporal summation - it arises when the same input stimulated in succession.

25
Q

benefit of indirect over direct synaptic transmission

A

NT in cleft longer –> extended action after NT action finished (ex= emotion)

2nd messengers transmit chemical signals to nucleus –> change gene expression

26
Q

example of first messenger doing double duty turning on fast and slow (direct/indirect)

A

autonomci ganglion receive cholinergic input from CNS –> ACh release –> ionotropic in NMJ –> NSC that depol

ACh activ metabotropic receptor in postsyn –> slower depol by closing K+ channels

27
Q

2 types of ACh receptors

agonist and antagonist

A

nictoinic ACh receptor
agonist = nicotine
antagonist = curare

muscarinic ACh receptor (GPCR)
agonist = muscarine
antagonist = atropine

28
Q

Define
Neostigmine
Curare (d-tubocurarine)

A

blocks ach esterase and prolongs current at NMJ (used for myasthenia gravis/syndrome)

Curare = block ACh receptor and induces paralysis; relaxant in anesthesia