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Neuroscience > CNS Neurotransmitters Lec05 > Flashcards

CNS Neurotransmitters Lec05 Flashcards

1
Q

What are the small molecule NT? *

A
  1. ach.
  2. amino acids – glutamate, gaba, glycine
  3. biogenic amines – dopamine, norepinephrine, serontonin
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2
Q

what are the amiunoacid NT?

A

gaba, gluamate, glycine

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3
Q

what are the biogenic amine NT?

A

dopamine, norepinephrine, serotonin

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4
Q

how many different neuropeptides are there

A

more than 100 different peptides

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5
Q

neuropeptides are typically ___ amino acids long

A

3-36

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6
Q

what are the two major classes of NT?

A

small moelcule and neuropetides

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7
Q

The concentration of neurotransmitter within the synaptic cleft is tightly controlled via regulation of:

A

synthesis, packaging, release, and removal

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8
Q

where are small moelcule NT made?

A

presynaptic terminal

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9
Q

how are small NT packaged into vesicles?

A

by specific transport proteins in the vesicle membrane

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10
Q

where are neuropeptide NT made and packaged?

A

within the cell body

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11
Q

how are vesicles of enruopeptides transported to the nerve terminal?

A

via fast axonal transport

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12
Q

___ neurotransmitters can respond very rapidly?

A

small molecule

are right there in the synaptic terminal to respond quickly

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13
Q

___ neurotransmitter release must be carefully regulated to prevent depletion.

A

neuropeptide

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14
Q

ionotropic receptors are ____ gated ion channels that open in response to ligand bonding

A

ligand gated

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15
Q

how many subunits do ionotropic chanels contain? how many transmembrane domains does each subunit contain?

A

5 subunits; 3-4 transmembrane domains

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16
Q

how is diversity established with ionotropic NT?

A

muleiple subunits are assembled in different orders

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17
Q

metabotropic coupled receptors activate ___ in response to ligand binding

A

g-proteins

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18
Q

activated G-proteins modulate ion channels either

A

directly or indirectly

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19
Q

how many transmembrane domains does each monmeric metabotropic receptor have?

A

7 transmembrane domains

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20
Q

what are the functions of acetylcholine in the CNS?

A

Attention, arousal, reward plasticity.
Enhances sensory functions upon waking

memory

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21
Q

Damage to cholinergic system is associated with the ___

A

memory defecits in AD

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22
Q

where is acetylcholien found in the peripheral NS?

A

NMJ

synapses in ganglia of the visceral motor system

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23
Q

how is AcH synthesized?

A

enzymatically in nerve terminal from acetyl-CoA and
choline

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24
Q

how is acetylcholine removed from the synaptic cleft?

A

via cleavage to acetate and choline by acetylcholinesterase

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25
Q

after degradation, how is more acetylcholine made?

A

choline is taken up by nerve terminal via a specific transporter and is used to synthesize more Ach

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26
Q

how are Organophosphates such as some insecticides and nerve gas hamrful to humans?

A

inhibit acetylcholinesterase causing ACh to accumulate at cholinergic synapses.

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27
Q

what is the result of organophasopates (nerve gases and insectisides) causing acetylcholine build up at the NMJ?

A

causes muscle paralysis

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28
Q

___ ach receptors mediate most acetylcholine effects in the brain?

A

metabotropic

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29
Q

scopolamine and atropine are

A

metabotropic achetylcholine anatagonists

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30
Q

what are the symptoms of myasthenia gravis?

A
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31
Q

with myasthenia gravis, patients have antibodies against

A

nicotinic acetylcholien receptors

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32
Q

how is the structure of the NMJ altered in myasthenia gravis

A
  1. dec concentration of acetylcholine receptors in postsynpatic membrane
  2. sparse and shallow junctional folds
  3. expanded synaptic cleft
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33
Q

size of ___ and ___ is reduced with myasthenia gravis

A

mini endplate potentials and endplate potentials

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34
Q

with myasthenai gravis, what is different during repeated stimualtion

A

the compound AP will be decreased in size (fatigue)

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35
Q

the probability of what is reduced with myasthenia gravis?

A

that a presynaptic AP will elicit a postsynatpci actioin potential

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36
Q

what does the tx of mysathenia gravis include?

A

cholinersterase inhbiitors

thyemactomy

corticoseteroids

immunosuppressants

37
Q

____ is the most prominent NT for normal brain function

A

glutamate

(more than half of all brain synapses use glutamate)

38
Q

____ has been shown to slowglutamate reuptake –> raising potential for neuroexoticity

A

oxygen depirvation

39
Q

why is glutamine important?

A

glutamate cannot cross blood brain barrier, but glutamine can

40
Q

how and where is gltuamate synthesized?

A

in the nerve terminal from

  1. glutamine
  2. the transamination of a-ketoglutarate
41
Q

how is glutamate removed from the synaptic cleft?

A

by high affinity glutamate transporters on both the nerve terminal and nearby glial cells

42
Q

what do glial cells do with gltuamate sucked up from the synaptic cleft?

A

glutamate is converted into glutamine and then transported out of the cell and back into nerve terminals

43
Q

___ binding is required to open NMDA channel

44
Q

__ ions can pass through NMDA channels

45
Q

Gaba is widely used where

A
  1. in the brain – 1/3 of all brain synapses use gaba
  2. in local interneurons and purkinje cells of cerebellum
46
Q

where is glyceine mostly used?

A

in the synapses in the spinal cord

47
Q

how is gaba synthesize?

A

in nerve terminals from glutamate

48
Q

what is needed for gaba to be made from glutamate?

A

pyridoxal phosphate (PLP) derived from vitamin B6

49
Q

how is gaba removed from the synaptic cleft?

A

by specific transporters on nerve terminals and nearby glia

50
Q

decreased gaba function can cause

51
Q

how is glyceine synthesized?

A

in nerve terminals from serine

52
Q

how is glycine removed from the synaptic cleft

A

by specific transporters on nerve terminals and nearby glia

53
Q

how can there be excess glycine? what can thise cause

A

defects in the glycine transporter can cause excessive glycine

excess glycine –> neonatal disease characterized by lethargy and mental retardation

54
Q

strychnine is a

A

glyceine receptor anatognist

55
Q

what are the effects of strychine

A

blocks gaba ionotropic receptors –> leads to overacitity int he spinal cord and brainstem –> seizures

56
Q

where are the biogenic amines made

A

in nerve terminals

57
Q

what packages the biogenic amines

A

vesicualr monoamine transporter (VMAT)

58
Q

how are the biogenic amines removed from the synaptic cleft

A

reuptake into nerve terminals

59
Q

what types of receptors do the biogenic amines ahve?

A
  • have metabotropic
  • serotonin has ionotropic as well
60
Q

how is dopamine made?

A

tyrospine –> dopa —> dopamine

61
Q

how is norepinephrine made?

A

tyrospine –> dopa —> dopamine –> norepinephrine

62
Q

how is epinephtrine made?

A

tyrospine –> dopa —> dopamine –> norepinephrine –> epinpeinphrine

63
Q

80% of brain dopamine found in ___

A

corpus striatum (which receives major input from the substantia nigra)

64
Q

midbrain dopamine system projections from the

A

ventral tegmental area to ventral parts of the striatum

65
Q

what is the midbrain dopamien system invovled in

A

motivation, reward, reinforcement

66
Q

what are doipamine projections tot he cortex involved in

A

emotional behavior

67
Q

norepinephrine neurons from the locus coerelus project to

A

forebriana nd brainstem targets

68
Q

what is the major transmitter of the sympathetic motor system

A

norepinehprine

69
Q

catehcolimine receptors are all

A

metabotropic

70
Q

anatagonists of ___ receptors in the medulla are sued as antiemtics

71
Q

dopamine receptors act by

A

activiating or inhbiitng adenyl cyclase

72
Q

dopamine blocks dopamine transports causing

A

a net increase in release of doapmine

73
Q

ampohetamine inhbiits both dopamine and norepeinphrine causing a

A

net increase in release of dopamine and norepinephrine

74
Q

raphe nuclei in the upper brainstem project to

A

forebrain and also to the brainstem

75
Q

how is serotonin transported back into the nerve terminal

A

by specific serotonin transporter or (SERT)

76
Q

metabotropic recpeotrs of serotonin are involved in

A

emotions, circadian rhtyms, motor behaviors, mental arousal

77
Q

activation of ___ mediates satiety and decreased food consumption

A

metabotropic serotonergic receptors

78
Q

MAO inhbiitors block the breakdown of

A

biogenic amines

79
Q

tricyclic antidperessants block the reuptake of

A

norepeinhprine and serotonin

80
Q

peptide NT are implicated in modulating

A

emotions, perceptions of pain, and repsonses to stress

81
Q

how are neuropeptides made?

A

synthesized as pre-propetides in the er in the cell body

82
Q

what are peptide nt sometimes co released with

A

small molecule NT

83
Q

how are neuropeptides degraded in the synaptic cleft

A
  1. removed by peptidases which degrade them
  2. degraded to more activ epeptides by endopeptidases
84
Q

metabotropic receptors of peptide NT are activated at ___ peptide concnetrations

A

relatively low

85
Q

morphine binds to the same receptors are

A

opoiud peptides

86
Q

which NT have just iontropic receptors

87
Q

what are the main functions of dopamine

A

coordiantion of body movement, movtivation, reward reinforcement

emotional behavior

88
Q

what can cause a neonatal disease characterized by lethargy and mental retardation?

A

excess glycine

Neuroscience (35 decks)

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