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Neuroscience > L 19 Mechanism of NT Release > Flashcards

L 19 Mechanism of NT Release Flashcards

1
Q

what is a NT?

A

chemical substance
synthesized in neurons
released at synapse following depolarization
binds to its respective receptor
elicits a response in the postsynaptic cell

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2
Q

what are the 3 main categories of NT in the nervous system?

A
  • small molecule transmitters
  • neuroactive peptide
  • gaseous NTs
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3
Q

what are some small molecule NT

A 
ACh
glutamate
GABA
glycine
doapine
NE
E
serotonin
histamine
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4
Q

what are some neuropeptides

A

orexins (hypocretins) - vasopressin + oxytocin

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5
Q

what are some gaseous NTs

A

Carbon monoxide

Nitric oxide

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6
Q

why don’t NO and CO fit all the definitions of NTs?

A
  • not stored in vesicles
  • don’t have calcium dependent release
  • doesn’t interaction with postsynaptic receptors
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7
Q

when is NO generated?

A

whenever it is needed - NO synthase needed for NO synthesis- nNOS is found in neurons

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8
Q

where are the enzymes for small molecule NT synthesized?

A

cytosol

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9
Q

where are the enzymes for small molecule NT stored?

A

clear vesicles bound to the cytoskeleton and await release at the active zone

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10
Q

where are neuropeptides synthesized?

A

soma

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11
Q

where are the neuropeptides stored?

A 
rough ER - enzymes + prepropeptides => pro peptides
Golgi - packaged into large dense core vesicles
Anterograde transport (kinesin)
terminal - propeptides cleaved into vesicles - neuropeptides stored in viscle on cutoskeleton
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12
Q

what does filing the synaptic vesicles depend on

A

est. gradient of H+ ions across the vesicular membrane

vesicular membrane has an antiport exhanging system - ex. exchanging dopamine for H+ ions

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13
Q

what are the two populations of vesicles?

A

clear vesicles - small molecule NT (ACh, glutamate)

Large dense cored vesicles - peptides (5-HT, NA)

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14
Q

what does a rise in [Ca2+] in terminal induce?

A

indirect phosphorylation of synapsin => untethers vesicle from the cytoskeleton

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15
Q

what does a local rise in [Ca2+] in the active zone facilitate?

A

opening of the inserted fusion protein allowing NT to leave the vesicle and enter the synaptic cleft

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16
Q

what is the falling phase?

A

removal mech. restoring the [Ca2+] to its normal low value

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17
Q

what is clearance of Ca2+?

A

Ca2+ ATPase and Ca2+/Na+ exchange systems extrude Ca2+ against its concentration gradient

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18
Q

where is calcium stored?

A

in sER, mitochondria, and other intracellular calcium stores

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19
Q

what is the role of synapsin

A

tethering the vesicle to the cytoskeleton

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20
Q

what is the role of Rab proteins

A

move vesicles towards the active zones for exocytosis

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21
Q

what is the role of SNARE

A

docking the vesicle with the nerves terminal membrane

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22
Q

what does the vesicular membrane have

A

v-SNARE (synaptobrevin and synaptotagmin)

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23
Q

what does the nerve membrane have

A

t-SNARE (syntaxin and neurexin)

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24
Q

synaptobrevin (v-SNARE) binds to?

A

syntaxin (t-SNARE)

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25
Q

synaptotagmin (v-SNARE) binds to?

A

neurexin (t-SNARE)

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26
Q

what is the role of synaptophysin?

A

binds to membrane cholesterol and forms the fusion pore in the nerve terminal membrane allowing transmitters to be released!

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27
Q

what are the steps in exocytosis of NT

A

mobilization
trafficking
docking
fusion

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28
Q

what promotes fusion

A

synaptobrevin + synaptotagmin + calcium + “complexin” cofactor

tSNARE complex = SNAP 25 + syntaxin

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29
Q

what does synaptophysin regulate?

A

quantal size of transmitter release in the nerve terminal membrane!

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30
Q

what happens at low nerve stimulation

A

rise in [Ca2+] occurs near the active zones ==> exocytosis of small clear vesicles containing small molecule transmitter

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31
Q

what happens at high nerve stimulation?

A

rise in [Ca2+] spreads far ==> exocytosis of large dense core vesicle containing peptides

32
Q

the same terminal can be used to release…

A

both transmitter types - peptides and small molecule transmitters

33
Q

all transmitters (except cholinergic transmitters) are ___ taken up back into nerve terminals, some are even absorbed by glial cells

A

rapidly

34
Q

how is the small clear vesicular membrane recovered?

A

slowly by endocytosis

35
Q

what is endocytosis responsible for the uptake of?

A

material (also viruses) from the extracellular fluid

36
Q

what is endocytosis of the small clear vesicular membrane mediated by?

A

clathrin - coats the vesicle

37
Q

once the vesicles are internalized, the vesicles lose their clathrin coats and fuse with the endosomes which form new vesicles to be ?

A

refilled with NTs

38
Q

how are dense core vesicles retrieved?

A

endocytosis – transported to soma by retrograde transport (dynein) for refilling with NTs

39
Q

define quantum

A

a packet of transmitter located in one synaptic vesicle

40
Q

define quantal size

A

the number of transmitter molecules in a quantum

quantal size of 7,000 molecules for synap. vesicles in motor n. ending
quantal size of 4,000 molecules for glutamate

41
Q

define quantum content

A

number of quanta released by a synaptic bouton under the influence of one invading impulse

42
Q

ACh is released from the motor nerve terminals in …

A

uniform packets = quanta- universal mechanism

43
Q

each vesicle containing a small molecule transmitter stores how many molecules?

A

4000-10,000 molecules of NT

44
Q

what is exocytosis governed by?

A

probability of release (p) and the number of vesicles available for release (n) = p x n

45
Q

what happens to the value of p (probability of release ) when an increase in [Ca2+]?

A

increase

46
Q

p (probability of release ) may be non-zero even in the absence of

A

stimulation of the nerve terminal

47
Q

what is the standard way to lower p (probability of release ) at the NMJ

A

replace Ca2+ with Mg2+ - it blocks the voltage gated Ca2+ channels –> decrease EPP

48
Q

when does EPP show quantal fluctuations?

A

when p has been reduced to a very low value

49
Q

what are miniature end plate potentials (minEPP)

A

Vm at the end plate, in the absence of nerve stimulation, show spontaneous small transient depolarizations about 1mV in size - indicate that the motor nerve terminal is releasing ACh spontaneously

50
Q

what are all EPPs

A

integral multiples of a unit size equal to that of a spontaneous minEPP

51
Q

the release of NT is

A

quantal

52
Q

what is the number of quanta released by a single impulse?

A

quantum constant

53
Q

what is the mean quantum content formula

A

(mean size of EPP) / (mean size of minEPP)

54
Q

what is the quantal hypothesis?

A

the presynaptic AP causes the release of the contents of an integral number of vesicles (1,2,3) and occasionally may fail to cause release of the contents of any vesicle

55
Q

what does botulinum toxin act as

A

protease - an enzyme that breaks down proteins and peptides.

56
Q

how does botulinum toxin work?

A

it binds to cholinergic nerve endings
enters and inactivated the docking mech. by breaking down synaptobrevin
prevents vesicular release of ACh irreversibly

57
Q

what is botulinum toxin used to tx?

A

dystonias (irregular or troublesome clonic contraction of muscles)
cosmetic surgery to reduce facial wrinkles.

58
Q

snake venom (beta-bungarotoxin) blocks what?

A

ACh release

59
Q

how does snake venom (beta-bungarotoxin) block ACh release?

A

binds irreversibly to actin and possibly other cytoskeleton components in cholinergic nerve endings and blocks ACh release
= paralysis and can be fatal is subject is not ventilated

60
Q

tetanus toxin blocks

A

glycine release

61
Q

how does tetanus block glycine release?

A

tetanus toxin has a protease component
it enters PNC via a cut or wound and passes into CNS by retrograde axonal transport
it enters glycinergic interneurons which inhibit firing of motor neurons where it inactivated docking of vesicles by breaking down synaptobrevin
it stops vesicular release of glycine irreversibly

62
Q

what are the symptoms of tetanus ?

A

powerful generalized muscle spasms

interference with respiration

63
Q

what is the tx for tetanus

A

neuromuscular blocking agents combined with assisted ventilation

64
Q

what does alpha-latrotoxin do?

A

depleted endings of cholinergic neurons

65
Q

how does alpha-latrotoxin work

A

black widow spider - promotes the fusion of cholinergic vesicles by binding to the neurexin/synaptotagmin complex
it induces a massive release of vesicular ACh that motor nerve terminals become depleted of synaptic vesicles

66
Q

what are the symptoms of alpha-latrotoxin poising?

A

muscle spasm followed by flaccid paralysis

ventilation may be necessary

67
Q

what is the role of aminoglycoside antibiotics - neomycin and steptomycin

A

inhibit exocytosis of ACh at motor nerve terminals by blocking presynaptic calcium channels

in high concentrations - can block postsynaptic nAChR

68
Q

which aminoglycoside antibiotic is more effective?

A

neomycin

69
Q

how are the effects of aminoglycoside antibiotics reversed?

A

increase extracellular calcium

70
Q

what does 4-aminopyridine do

A

K+ channel blocking drug prolongs the duration of the impulse and enhances Ca2+ entry into the motor nerve ending and raising the probabiltiy of ACh release and then the quantum content

71
Q

how do neurotransmitters alter quantum release?

A

at certain axo-axonic synapses the presynaptic inhibitory ending releases a transmitters (GABA, seratonin, dopamine) which binds to receptors in the membrane of the second (postsynaptic) cells and reduces its transmitter release
such axo-axonic synapses are common on the terminals of afferent neurons in the spinal cord

72
Q

what drugs alter quantum release?

A

aminoglycoside antibiotics
4-aminopyridine
neurotransmitters

73
Q

what is hypocalcemia - what causes it and what is it?

A

hypoparathyroidism causes hypocalcemia - lower blood concentration of calcium ions

74
Q

what are the symptoms of hypocalcemia?

A

tetany and paresthesias due to repetitive firing of AP in peripheral motor and sensory fibers

75
Q

why does low [Ca2+] cause repetitive firing?

A

extracellular calcium is needed to neutralize the negative charges in the extracellular matrix so its in its absence, the outside becomes more negative which makes the membrane different from outside to inside will get close to threshold which will cause eventual unwanted depolarizations

76
Q

motor nerve endings release about ___quanta of ACh in response to an invading impulse, but all other nerve endings usually release just ___ quanta

A

200

a few

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