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Physiology 1 (WPH) > L6: synaptic transmission > Flashcards

L6: synaptic transmission Flashcards

1
Q

why won’t an electric current transmit across a synapse?

A

it will dissipate in the extracellular space

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2
Q

what kind of junction permits transmission of an electric current between cells?

A

gap junction

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3
Q

what proteins make a gap junction and what structure do they form?

A

6 connexins around a central pore make a hemichannel (2 hemichannels come together to form a gap junction)

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4
Q

how is an electrical synapse formed?

A

through gap junctions

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5
Q

why aren’t electrical synapses the predominant form of communication in the nervous system?

A

electrical communication not always viable - e.g. current from a small fiber is insufficient to bring larger post-synaptic effector cells to threshold potential

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6
Q

what kind of synapses constitute the predominant form of communication in the nervous system?

A

chemical synapses

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7
Q

3 key functional differences between electrical and chemical synapses

A

chemical synapses:

  • one-directional (NT on one side, recepter on other)
  • synaptic delay (signal converted and back)
  • modulated (allowed by multiple steps)
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8
Q

typically how long is the synaptic delay in a chemical synapse?

A

0.5 - 1 ms

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9
Q

motor end-plate

A

the post-synaptic receptor region of a muscle cell

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10
Q

interstitial [Ca++]

A

~2 mM

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11
Q

intracellular [Ca++]

A

10^-4 mM

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12
Q

voltage-gated Ca++ channels are confined to the terminal region of the pre-synaptic axon called the…

A

active zone

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13
Q

why is Ca++ ideally suited to play the role of internal messenger in synaptic NT release?

A

Ca++ has a very large out vs in concentration gradient (2 vs 10^-4 mM)

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14
Q

EPP =

A

end plate potential

post-synaptic local potential in neuromuscular junction

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15
Q

MEPP =

A

miniature end-plate potential

cause by spontaneous release of an NT vesicle into neuromuscular junctoin

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16
Q

how many molecules in a quantum of neurotransmitter?

A

2,000 to 10,000

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17
Q

how can a comparable MEPP be experimentially induced?

A

by reducing the EPP with a solution of low Ca++ and high Mg++, which is a competitive inhibitor to Ca++ binding

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18
Q

why is neurotransmission “quantal”

A

neurotransmitter is released from vesicles in packets

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19
Q

T/F an MEPP reflects one quantum of neurotransmitter

A

true

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20
Q

roughly how many quanta are released in the neurotransmission of a signal

A

a few hundred

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21
Q

what class of proteins regulate the process of NT exocytosis?

A

SNARE proteins

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22
Q

synapsin’s role in in neurotransmission

A

tether NT vesicles at the ready to cytoskeletal structures

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23
Q

synaptobrevin’s role in neurotransmission

A

in NT vesicle membrane, docks vesicle to syntaxin on the plasma membrane release site

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24
Q

syntaxin’s role in in neurotransmission

A

in presynaptic plasma membrane, tethers with synaptobrevin on the NT vesicle membrane to dock vesicle at release site

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25
Q

synaptotagmin’s role in in neurotransmission

A

senses Ca++ elevation and triggers NT vesicle fusion

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26
Q

why is NT vesicle release a “kiss & run” process

A

synaptic vesicles fuse, release contents, and retract back into synapse to be refilled and reused

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27
Q

SNAP25’s role in in neurotransmission

A

executes fusion of NT vesicle

plasma membrane bound, similar to syntaxin

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28
Q

what are the roles of the following SNARE proteins in neurotransmission:

  • synapsin
  • synaptobrevin
  • syntaxin
  • SNAP25
  • synaptotagmin
A
  • synapsin: tether vesicles to cytoskeleton
  • synaptobrevin: on VM, docks to PM
  • syntaxin: on PM, docks vesicle
  • SNAP25: on PM, executes fusion
  • synaptotagmin: binds Ca++, triggers fusion
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29
Q

3 main pathways for neurotransmitter removal from synaptic cleft

A
  • diffusion
  • degradation
  • re-uptake
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30
Q

ACh-E

A

acetylcholinesterase

-hydrolyzes ACh into acetate and choline

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31
Q

what is the enzyme that breaks down ACh in the synaptic cleft?

A

ACh-E

acetylcholinesterase

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32
Q

what are the products of ACh-E hydrolysis of ACh?

A

acetate

choline

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33
Q

does ACh-E reside free in the synaptic cleft or on the post-synaptic membrane?

A

it varies, depicted either way

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34
Q

what is the rate of ACh hydrolysis by ACh-E in the synaptic cleft?

A

~40,000 ACh/s

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35
Q

how is NT re-uptake accomplished?

A

through Na+ coupled transporters

secondary active transport

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36
Q

what are two types of NT receptors on post-synaptic membranes?

A

ionotropic receptors

metabotropic receptors

37
Q

are nicotinic receptors ionotropic or metabotropic?

A

ionotropic

38
Q

nicotinic receptors bind which NT?

A

ACh

39
Q

how does an ionotropic NT receptor work?

A

NT binding causes conformational shift and opening or closing of a path for ions to flow

40
Q

what kind of NT receptor is appropriate for fast-acting effects, e.g. “run for your life!”

A

ionotropic

41
Q

what kind of NT receptor is appropriate for sustained effects, e.g. slowing heart rate for sleeping

A

metabotropic

42
Q

what is the advantage/disadvantage of ionotropic receptors?

A

fast acting / no amplification or modulation

43
Q

how do metabotropic NT receptors work?

A

NT binding induces activation of second messenger proteins and an enzyme reaction chain that results in opening of ion channels

44
Q

what is the typical first link in a metabotropic NT receptor chain

A

G-protein

45
Q

are serotonin receptors ionotropic or metabotropic?

A

metabotropic

46
Q

how do G-proteins usually work

A

G-protein activation causes release of GDP and binding of GTP, which causes α subunit to dissociate from βγ complex, and subunits are now available to interact with effector proteins, typically producing second messengers. the G-protein resets after GTP has been hydrolized and α regroups with βγ

47
Q

what is the advantage / disadvantage of metabotropic NT receptors?

A

amplification & modulation / sluggish

48
Q

what kind of potential is activated by NT binding to post-synaptic receptors?

A

local potential

49
Q

T/F NT receptors are mostly located at the junctional region

A

true

50
Q

what is the effect of adding the poison d-turbocurarine to the synapse?

A

blocks ACh receptors

51
Q

T/F the machinery that converts an electrical response to a chemical signal and back is all confined to the synaptic region

A

true

52
Q

what is a reversal potential

A

an experimentally clamped ∆V at which a NT-receptor binding and opening of ion channels causes no net change in current flow across membrane – this ∆V reversal depends on what ions the opened channels are permeable to, and how permeable it is to these ions
I net = I1 + I2 +… = 0
g1 (V1 - E1) + g2 (V2 - E2) + … = 0

53
Q

what is the Na+ / K+ permeability of ACh opened channels?

A

1.25

54
Q

if reversal potential = -15 mV and the NT opened channels are permeable to Na and K, what is the ratio of Na+ / K+ permeability in the channels?

A 
I net = I Na + I K = 0 (at reversal potential)
g Na (V - E Na) + g K (V - E K) = 0
g Na (-65) + g K (80) = 0
g Na / g K = 80/65 = 1.23
55
Q

EPSP =

A

excitatory post-synaptic potential

56
Q

NT opened channels with ∆V reversal < ∆V resting will produce what kind of post-synaptic potential?

A

IPSP
inhibitory post-synaptic potential
(hyperpolarizing)

57
Q

NT opened channels with ∆V reversal > ∆V resting will produce what kind of post-synaptic potential?

A

EPSP
excitatory post-synaptic potential
(depolarizing)

58
Q

EPSP =

A

excitatory post-synaptic potential

depolarizing

59
Q

IPSP =

A

inhibitory post-synaptic potential

hyperpolarizing

60
Q

T/F reversal potential = threshold potential

A

false - reversal potential is the equilibrium potential of NT opened channels, which indicates whether an NT effect will produce an EPSP (∆V rev > ∆V rest) or an IPSP (∆V rev < ∆V rest)

61
Q

what are two inhibitory synapse mechanisms?

A

hyperpolarize

stabilize

62
Q

how can an inhibitory synapse function without producing and IPSP?

A

synaptic inhibition can be achieved by opening channels permeable to an ion with an equilibrium potential near V resting (e.g. Cl-); this will make conductance to Cl- dominant and will clamp the ∆V resting near E Cl-, resisting change in ∆V from that value

63
Q

equilibrium potential of Cl- =

A

~-65 mV

-61log(112/10)

64
Q

T/F a given NT always elicits the same post-synaptic response (excitatory or inhibitory)

A

false - dependent on the receptors and ion channels involved, a given NT can produce EPSPs or IPSPs in different circumstances

65
Q

name the 6 major classes of amino acids

A 
ACh
biogenic amines
amino acids
neuroactive peptides
gases
purines
66
Q

4 biogenic amines that function as neurotransmitters:

A

norepinephrine
dopamine
serotonin
histamine

67
Q

4 amino acids that function as neurotransmitters:

A

glutamate
aspartate
GABA
glycine

68
Q

2 gases that function as neurotransmitters:

A

NO

CO

69
Q

2 purines that function as neurotransmitters:

A

ATP

Adenosine

70
Q

T/F in the neuromuscular junction the post-synaptic response to a Single nerve impulse is sufficiently large to activate voltage-gated Na+ and K+ channels and initiate an action potential

A

true
(while true at the neuromuscular junction, this is not the case in a typical nerve cell, which sums many EPSPs and IPSPs)

71
Q

why is the neuron a center of integration, and not just a simple relay link along a chain?

A

the dendritic tree and soma of the cell do not contain the density of voltage gated Na+ and K+ channels to initiate and action potential – this machinery exists at the axon hillock and down the axon, where the local potentials of the dendrites and soma are summed and an action potential is initiated (or not)

72
Q

where in the neuron is the density of V-gated Na+ channels sufficient to initiate and action potential?

A

-axon hillock and axons

not dendritic tree and soma

73
Q

how does τ change over the course of a post-synaptic local potential (EPSP or IPSP) ?

A

τ is shorter when channels open (Rm decreases)
τ is longer when channels close (Rm increases)
so the ∆V has a quick spike and a slow return to rest

74
Q

temporal summation

A

burst of PSPs over a short period can summate and reach a larger ∆V even though individual PSPs may be quite small

75
Q

spatial summation

A

two or more PSPs from different locations converging on the same neuron can add up in magnitude to reach a larger ∆V even though individual PSPs may be much smaller

76
Q

2 factors that can help a PSP reach the axon hillock with greater amplitude

A
  • proximity to hillock

- diameter of fiber (lower τ higher λ)

77
Q

what is the ICF / ECF ratio of:
Cl-
Ca++

A

Cl-: 10 / 112

Ca++: 10^-4 / 2

78
Q

T/F inhibitory synapses often occur on the cell body because this is where they are most effective in preventing an action potential from occurring

A

true

79
Q

T/F spatial summation may occur between an inhibitory and excitatory local potential

A

true

80
Q

T/F temporal summation occurs between EPSPs generated by one synapse

A

true

81
Q

T/F spatial and temporal summation of excitatory local potentials is less likely if the membrane has more leakage channels

A

true

82
Q

T/F temporal summation is more likely if the membrane capacitance is low

A

false - if membrane capacitance is low, τ = RmCm will be low, conduction velocity will be high, and an EPSP will be more likely to run away along the membrane too quickly for the next EPSP to catch it and summate.

83
Q

when axon radius decreases, how does this affect the ∆V τ and λ ?

A

no change τ = RC ~1/A x A

decrease λ ~ sq.rt (r) (Rm~1/A; Ri~1/Vol)

84
Q

when axon radius increases, how does this affect ∆V τ and λ ?

A

no change τ = RC ~1/A x A
increase λ ~ sq.rt (r)
(because Rm~1/A; Ri~1/Vol)

85
Q

T/F EPSPs can temporally summate at a single synapse to yield a membrane potential more positive in value than any one EPSP

A

true

86
Q

T/F ACh muscarinic receptors are the target of circulating antibodies in myasthenia gravis

A

false
nicotinic receptors at neuromuscular junctions
(probably N1)

87
Q

T/F acetylcholine is the major transmitter released from post-ganglionic sympathetic fibers

A

false - ACh and NE are both major transmitters released from post-ganglionic sympathetic fibers
(ACh is major NT released from somatic motor fibers)

88
Q

T/F the channel opened by acetylcholine in the muscle endplate is selective to Na+ and K+

A

true (though a little more selective for Na+)

Physiology 1 (WPH) (18 decks)

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