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MOVEMENT NEUROSCIENCE EXAM 1 > MODULE 3- Synaptic Transmission > Flashcards

MODULE 3- Synaptic Transmission Flashcards

1
Q

2 mechanisms of synaptic signaling

A

-chemical synapses
-electrical synapses

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2
Q

chemical synapses

A

use neurotransmitters + their receptors
-Ca2+ dependent neurotransmitter release

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3
Q

chemical synapses are unidirectional/bidirectional

A

unidirectional

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4
Q

chemical synapses are slow/fast

A

slow

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5
Q

chemical synapses- what do ions flow through

A

postsynaptic channels

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6
Q

electrical synapses

A

use gap junctions as ion channels

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7
Q

electrical synapses are unidirectional/bidirectional

A

bidirectional

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8
Q

electrical synapses are slow/fast

A

fast

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9
Q

electrical synapses- what do ions (current) flow through

A

connexon channels

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10
Q

synaptic delay between 2 cells at electrical synapses

A

less than 0.1 msec

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11
Q

hippocampal interneurons

A

one of the few places in the CNS that use electrical synapses

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12
Q

due to the bidirectional transmission of electrical synapses, generation of APs in one neuron results in what

A

synchronized firing of APs in the adjacent neuron

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13
Q

electrical synapses- what happens as current sweeps across tissue

A

entire tissue can be stimulated virtually simultaneously as the current sweeps across it

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14
Q

key hallmark feature of chemical synapses

A

use of a chemical neurotransmitter

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15
Q

ultimately, what is the AP in the postsynaptic neuron generated by

A

the opening of ion channels
-which changes the membrane potential
-achieved through either ionotropic or metabotropic receptors

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16
Q

3 criteria of a neurotransmitter

A

-must be present in the presynaptic neuron
-must be released during synaptic activity
-must bind receptors on the postsynaptic neuron

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17
Q

co-transmitters

A

sometimes a neuron can synthesize + release more than 1 type of neurotransmitter

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18
Q

steps of a chemical synapse

A

transmitter is synthesized + then stored in vesicles ->

an AP invades the presynaptic terminal ->

depolarization of presynaptic terminal causes opening of voltage-gated Ca2+ channels ->

influx of Ca2+ through channels ->

Ca2+ causes vesicles to fuse with presynaptic membrane ->

transmitter is released into synaptic cleft via exocytosis ->

transmitter binds to receptor molecules in postsynaptic membrane ->

opening or closing of postsynaptic channels ->

postsynaptic current causes excitatory or inhibitory postsynaptic potential that changes the excitability of the postsynaptic cell ->

removal of neurotransmitter by glial uptake or enzymatic degradation ->

retrieval of vesicular membrane from plasma membrane

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19
Q

what do calcium ions regulate

A

the release of discrete packets of neurotransmitters

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20
Q

what does synaptic transmission at the NMJ result in

A

end-plate potentials (EPPs)

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21
Q

what do spontaneous firings in the muscle cell result in

A

miniature EPPs (MEPPs)

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22
Q

what is equivalent to a MEPP

A

ACh released in discrete packets

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23
Q

what do EPPs represent

A

many simultaneous MEPP-like units

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24
Q

train of presynaptic APs causes what

A

rise in Ca2+
-tracked by Ca2+ dependent fluorescent dye

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25
Q

what does microinjection of Ca2+ chelator into presynaptic terminal prevent

A

prevents transmitter release + therefore postsynaptic APs

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26
Q

what does increasing presynaptic [Ca2+] do

A

causes neurotransmitter release from presynaptic terminals

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27
Q

what is responsible for neurotransmitter release

A

a cycle of membrane trafficking

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28
Q

quantal release of neurotransmitters

A

-individual quanta of neurotransmitters are caused by the fusion of the vesicle memrbane with the plasma membrane
-number of quanta released is positively correlated with the number of vesicles fusing

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29
Q

average synaptic vesicle diameter

A

~ 50 nm
-corresponding to 100 mM of ACh

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30
Q

myasthenic syndromes affect which terminal

A

presynaptic

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31
Q

myasthenic syndromes

A

abnormal transmission at neuromuscular synapses
-leads to weakness + fatigue at skeletal muscles

32
Q

what 3 things can myasthenic syndromes affect

A

-acetylcholinesterase
-cholinergic receptors
-voltage-gated Ca2+ channels (VGCC)

33
Q

Lambert-Eaton myasthenic syndrome

A

loss of VGCCs (voltage-gated Ca2+ channels)

34
Q

myasthenia gravis

A

an autoimmune disease that produces antibodies against nicotininc ACh receptors at the NMJ
-produces weakness + fatigue
-produces much smaller EPPs + MEPPs than in unaffected people

35
Q

how can myasthenia gravis be improved

A

with acetylcholinesterase inhibitors, such as neostigmine
-this would increase the concentration of ACh in the synapse

36
Q

what is the “protocol neurotransmitter”

A

ACh

37
Q

what was the 1st neurotransmitter to be discovered

A

ACh

38
Q

**what is ACh derived from

A

-acetyl-CoA
-choline

39
Q

**what does acetylcholinesterase metabolize ACh into

A

-acetate
-choline

40
Q

acetylcholinesterase efficiency

A

extremely efficient
-5,000 ACh metabolized per second

41
Q

2 families of neurotransmitter receptors

A

-ligand-gated ion channels
-metabotropic receptors

42
Q

ligand-gated ion channels are also called

A

ionotropic receptors

43
Q

ligand-gated ion channels (ionotropic receptors)

A

receptor itself is also the ion channel

44
Q

ligand-gated ion channels (ionotropic receptors) are slow/fast

A

fast
-postsynaptic potentials responses range 1-2 msec after an AP reaches the presynaptic terminal

45
Q

metabotropic receptors are also called

A

G-protein-coupled receptors

46
Q

metabotropic receptors (G-protein-coupled receptors)

A

G-protein complex is activated by ligand binding to the receptor

47
Q

metabotropic receptors (G-protein-coupled receptors) are slow/fast

A

slow
-postsynaptic potentials responses range from hundreds of msec to 1-2 min

48
Q

steps of ligand-gated ion channels

A

neurotransmitter binds ->
channel opens ->
ions flow across membrane

49
Q

steps of metabotropic receptors

A

neurotransmitter binds ->

G-protein is activated ->

G-protein subunits or intracellular messengers modulate ion channels ->

ion channel opens ->

ions flow across membrane

50
Q

what changes during synaptic transmission

A

postsynaptic membrane permeability

51
Q

what opens ligand-gated ion channels when binding to its receptors

A

ACh

52
Q

end-plate current (EPC)

A

results when thousands of ACh receptors are opened as a result of the ligand binding to the former

53
Q

EPC is an inward/outward current

A

inward current
-causing a depolarization or postsynaptic AP
-caused by the influx of Na+ and subsequent efflux of K+

54
Q

what is EPC caused by

A

influx of Na+ and subsequent efflux of K+

55
Q

**reversal potential (E rev)

A

the voltage at which direction of the current changes from outward to inward

56
Q

what does reversal potential (E rev) reveal

A

the identity of the ions pemeating the postsynaptic receptors

57
Q

what is reflected by the reversal potential of the EPC

A

permeability to any particular ion
-would be at the equilibrium potential for that ion

58
Q

describe permeability of ACh-activated ion channels compared to Na+ and K+

A

ACh-activated channels are almost EQUALLY permeable to both Na+ and K+
-shown by the findings that EPCs reverse at 0 mV

59
Q

what do postsynaptic ion fluxes determine

A

determine whether synapses are excitatory or inhibitory

60
Q

**excitatory postsynaptic potentials (EPSPs)

A

increase the likelihood of a postsynaptic AP

61
Q

glutamate is an EPSP/IPSP

A

EPSP

62
Q

EPSPs allow for influx of what ion

A

Na+ influx

63
Q

inhibitory postsynaptic potentials (IPSPs)

A

decrease the likelihood of a postsynaptic AP

64
Q

GABA is an IPSP/EPSP

A

IPSP

65
Q

IPSPs allow for the influx + efflux of which ions

A

either Cl- influx or K+ efflux

66
Q

EPSPs have ____ strength

A

subthreshold strength
-not enough to generate an AP

67
Q

IPSPs of equal subthreshold strength can do what to an EPSP

A

cancel out EPSP

68
Q

what happens to all converging EPSPs + IPSPs stimulating a postsynaptic neuron

A

added together in both space + time

69
Q

summation of synaptic potentials- space

A

how far away are each of them (synapse) from the axon hillock?

70
Q

summation of synaptic potentials- time

A

how long does it take each PSP to reach the axon hillock?

70
Q

if the combined strength (in mV) of PSPs reaches threshold…

A

an AP will fire + be transmitted down the axon

71
Q
A
72
Q

what does convergence of hundreds or thousands of presynaptic inputs across the soma + dendritic spines lead to

A

summation

73
Q

as a result of summation across space + time, what do changes in membrane potential depend on

A

whether it reaches threshold

74
Q

overview of postsynaptic signaling

A

neurotransmitter release ->

receptor binding ->

ion channels open or close ->

conductance change causes current flow ->

postsynaptic potential changes ->

postsynaptic cells excited or inhibited ->

summation determines whether or not an AP occurs

MOVEMENT NEUROSCIENCE EXAM 1 (9 decks)

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