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Neuroscience - Unit 5 > Lecture 5- CNS Neurotransmitters > Flashcards

Lecture 5- CNS Neurotransmitters Flashcards

1
Q

list 7 of the most important small molecule neurotransmitters.

A

acetylcholine, glutamate, GABA, glycine, dopamine, norepinephrine and serotonin

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2
Q

how many different neuropeptides are there and how large are they?

A

over a hundred

typically 3-36 AA long

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3
Q

how is the concentration of neurotransmitter in the synaptic cleft regulated?

A

neurotransmitter synthesis, packaging, release and removal

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4
Q

what terminates synaptic transmission?

A

removal of the NT from the synaptic cleft

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5
Q

where are small molecule and neurotransmitters synthesized and packaged? what implication does this have on replenishment in times of increased demand?

A

small molecule- in the nerve terminal
neuropeptides- in the soma
small molecules are quickly made to be distributed while it takes longer for peptide synthesis and transport

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6
Q

why can small molecule NT synthesis be called slower than peptide NT synthesis?

A

because, initially the protein making machinery must be made in the soma and transported to the nerve terminal

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7
Q

describe the structure of an ionotropic neurotransmitter receptor.

A

ligand gated ion channels that consist of 4 or 5 subunits with 3-4 transmembrane domains each

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8
Q

what causes the diversity of receptors for a single neurotransmitter?

A

multiple different types of subunits

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9
Q

describe the structure of metabotropic receptors.

A

they are G protein coupled receptors that are monomeric and contain 7 transmembrane domains

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10
Q

how are metabotropic and ionotropic receptors similar in their effect?

A

modulation of ion channels

metabotropic receptors modulate ion channels directly or indirectly

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11
Q

what do the different subunits of ionotropic receptors contribute to?

A

they give the receptor distinct properties

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12
Q

what are the two main contributing factors to diversity of metabotropic receptors?

A

the receptor type and the G protein that it is coupled to

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13
Q

where is acetylcholine present in the peripheral nervous system?

A

at the neuromuscular junction and in the synapses of ganglia in the autonomic nervous system

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14
Q

in what two locations is ACh found in the CNS?

A

in interneurons in the brainstem and forebrain and in large neurons in the basal forebrain that project to the cerebral cortex

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15
Q

what are the four CNS functions of ACh?

A

in attention, arousal, reward plasticity and enhancing sensory functions upon waking

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16
Q

describe the synthesis and packaging of ACh.

A

synthesize din nerve terminal from acetyl CoA and choline and packaged into synaptic vesicles by an ACh transporter

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17
Q

what happens to ACh after it is released into the synaptic cleft?

A

it is cleaved by acetylcholinesterase into acetate and choline. the choline is taken back into the nerve terminal and recycled

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18
Q

what poison inhibits ACh function and how?

A

organophosphates such as sarin gas inhibits AChE and causes ACh accumulation at the synapse. results in muscle paralysis because the continued depolarization of the postsynaptic cell makes it refractory

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19
Q

which ACh receptors are ionotropic and which are muscarinic? where are they located?

A

ionotropic- nicotinic; located in the neuromuscular junction and in CNS
metabotropic- muscarinic; in the forebrain and peripheral ganglia of the autonomic nervous system

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20
Q

what are two muscarinic antagonists that can be used therapeutically?

A

atropine-pupil dilation

scopolamine- for motion sickness

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21
Q

what are the symptoms of myasthenia gravis?

A

muscle fatigability worsening late in the day and improving with rest, diploplia, ptosis, and difficulty with speaking and swallowing

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22
Q

what is the cause of myasthenia gravis?

A

antibodies directed against the muscular nicotinic receptors decreasing their quantity

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23
Q

what are three differences of the NMJ in patients with myasthenia gravis?

A

decreased concentration of ACh receptors, sparese and shallow junctional folds and an expanded synaptic cleft

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24
Q

what is the effect myasthenia gravis on muscle function?

A

decreases the size of MEPP and EPP’s, decreases the probability of muscular action potential. the action potential decreases in size during repeated stimulation

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25
Q

what are four treatments of myesthenia gravis?

A

cholinesterase inhibitors, thymectomy, corticosteroids and immunosuppressants

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26
Q

what is the most prominent transmitter for normal brain function?

A

glutamate

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27
Q

what problem can glutamate cause to neurons?

A

can cause excitotoxicity which can excite a neuron to death

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28
Q

when is excitotoxicity most often seen? what can be used to prevent it?

A

thought to cause damage during stroke when oxygen deprivation slows glutamate reuptake. may be treated with glutamate receptor antagonists in the future

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29
Q

what is glutamate synthesized from and where? why is it not just transported into the cell?

A

synthesized from glutamine or by the transamination of alpha ketoglutarate in the nerve terminal. glutamate cannot cross the blood brain barrier

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30
Q

what happens to glutamate after it is released into the synapse?

A

it is removed by high affinity transporters in the nerve terminal and nearby glial cells. the glial cells convert the glutamate back into glutamine and transport it back into the nerve terminal

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31
Q

what are the three different types of ionotropic glutamate receptors? what types of channels are they?

A

NMDA, AMPA and kainate

they are excitatory Na+ channels

32
Q

what is unique about NMDA receptors?

A

Ca++ can pass through, ion flow is ligand and voltage dependant because of the Mg++ blocking entry and glycine is also required to open the channel

33
Q

what is the result of metabotropic activation by glutamate?

A

either activation or inhibition of the postsynaptic cell

34
Q

what are the major inhibitory transmitters in the CNS? where are they primarily used?

A

GABA is widely distributed in the brain and within the interneurons and purkinje cells of the cerebellum.
glycine is used at synapses in the spinal cord predominantly

35
Q

where is GABA synthesized and what does it require?

A

it is synthesized in nerve terminals from glutimate

requires pyridoxal phosphate (PLP) derived from vitamin B6

36
Q

how is GABA removed from the synaptic cleft?

A

it is removed by transporters on the nerve terminal and nearby glial cells. GABA-T then returns it to glutamine

37
Q

what does decreased GABA function cause?

A

epilepsy

38
Q

what is glycine synthesized from and what transporter does it share with GABA?

A

it is synthesized from serine and packaged into vesicles by the vesicular inhibitory amino acid transporter (same as GABA)

39
Q

how is glycine removed from the synapse and what is a consequence of its failure?

A

removed into nearby glia and the nerve terminal

excess synaptic glycine causes neonatal disease with lethargy and mental retardation

40
Q

what are the ionotropic and metabotropic GABA receptors?

A

ionotropic- GABA a and GABA c

muscarinc- GABA b

41
Q

what types of channels are GABA and glycine receptors?

A

inhibitory chloride channels

42
Q

what are two GABA receptor agonists and what are they use for?

A

benzodiazopine is used as a tranquilizer

barbiturates are used as anesthetics to control epilepsy

43
Q

what is a glycine receptor antagonist and what does it do?

A

strychnine (used in rat poison)- causes over activity in the spinal cord and brainstem leading to seizures

44
Q

what is the distribution of expression of GABA and glutamate receptors and synthesizing molecules?

A

both are expressed broadly across the brain

45
Q

what is the distribution of expression of Dopamine, Norepinephrine and Serotonin receptors and synthesizing molecules?

A

the receptors are widely distributed while the synthesizing machinery is only expressed in localized regions

46
Q

what are the three catecholamines and what other neurotransmitters are part of the group of biogenic amines?

A

catecholamines: dopamine, epinephrine and norepinephrine
rest: histamine and serotonin

47
Q

what is the main function of aminergic neurons?

A

to help modulate the intensity of more specific neuronal signals- only used by a few neurons in the brain

48
Q

what transporter packages biogenic amines and where are they removed to after use?

A

vesicular monoamine transporter

reuptake into nerve terminals

49
Q

what type of receptors do biogenic amines utilize and what is the exception?

A

metabotropic

serotonin also has ionotropic receptors

50
Q

describe catecholamine synthesis.

A

tyrosine->DOPA->dopamine->NE->epinephrine

51
Q

describe serotonin synthesis.

A

tryptophan-> 5-hydroxytryptophan->serotonin

52
Q

where are dopamine containing neurons and what are their functions?

A

substantia niagra->striatum: coordination of body movements
midbrain (ventral tegmental area->ventral parts of striatum): involved in motivation, reward and reinforcement
projections to the cortex (minor): emotional behavior

53
Q

what type of neurons degenerate in Parkinsons and what is it treated with?

A

dopamine neurons in the substantia nigra and they are treated with L-DOPA (precursa to dopa)

54
Q

what do addictive drugs such as cocaine do?

A

raise dopamine levels by interfering with reuptake

55
Q

where are NE containing neurons in the CNS and PNS and what is the function?

A

CNS: from the locus coeruleus- influences sleep and wakefulness, attention and feeding
PNS: sympathetic ganglion cells- transmitter of synaptic motor system

56
Q

what type of receptors do catecholamines use?

A

metabotropic

57
Q

what do dopamine receptors do and what are antagonists used for?

A

they activate or inhibit adenylyl cyclase

antagonists used as anti-emetics

58
Q

whaqt are antagonists and agonists of norepinephrine used for and where do they have effect?

A

they are used for cardiac arrhythmias and migraine headaches and they are mediated by receptors in smooth muscle

59
Q

how are catecholamines removed from the synaptic cleft?

A

by using transmitter specific plasma membrane transporters into nerve terminals and glia

60
Q

what is the effect of amphetamine?

A

it inhibits both dopamine and norepinephine transporters

61
Q

where are serotonin containing neurons and what do they do?

A

in the raphe nuclei projecting to the forebrain and brainstem
implicated in regulation of sleep, eating, arousal and wakefullness

62
Q

what transporter reuptakes serotonin? what is it inhibited by?

A

SERT

SSRIs

63
Q

what are metabotropic serotonin receptors implicated in?

A

emotions, circadian rhythms, motor behaviors and mental arousals.
impaired in psychiatric disorders
activation mediates satiety

64
Q

describe ionotropic serotonin receptors and what is one reason a drug would target them?

A

non selective excitatory cation channels

target for drug to prevent nausea

65
Q

what do antipsychotic drugs do?

A

block dopamine receptors because excess dopamine release may cause some psychotic illnesses

66
Q

what is the goal of two subtypes of anti-anxiety drugs?

A

MAO inhibitors block breakdown of biogenic amines

some are inhibitors of serotonin reuptake

67
Q

what are the three classes of antidepressants?

A

MAO inhibitors that block the breakdown of biogenic amines
tricyclic antidepressents block reuptake of serotonin and NE
serotonin reuptake inhibitors act on serotonin transporters specifically

68
Q

what effects do peptide neurotransmitters have? what is their biological activity dependent upon?

A

modulate emotions, change pain perception and responses to stress
dependent upon the amino acid sequence

69
Q

what are the five categories of peptide neurotransmitters?

A

brain-gut peptides, opioid peptides, pituitary peptides, hypothalamic releasing peptides and miscellaneous peptides

70
Q

describe the synthesis and processing of neuropeptides.

A

synthesized in ER and processed there. final processing into active peptides occurs in the vesicles after they bud off of the Golgi (multiple different active peptides)

71
Q

describe the release and removal of neuropeptides from the synaptic cleft.

A

coreleased with small-molecule neurotransmitters and removed from the cleft via degradation by peptidases

72
Q

what sometimes happens to peptide NTs within the synaptic cleft?

A

they are degraded to more active peptides

73
Q

what is the affinity of peptide receptors?

A

they are activated at relatively low peptide concentrations

74
Q

where are opioid peptides and what are their functions?

A

wide distribution throughout brain

tend to be depressants and can act as analgesics

75
Q

what is morphine and what does it do?

A

it is an opioid that is an analgesic

it binds to the same receptors as opioid peptides

Neuroscience - Unit 5 (12 decks)

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