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neuroscience > CNS neurotransmitters > Flashcards

CNS neurotransmitters Flashcards

1
Q

what are the 2 major types of neurotransmitters?

A

small molecules ( classic neurotransmitters) and neuropeptides

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2
Q

name the three main types and examples of other small molecule ( classical neurotransmitters)

A

acetylcholine (ACh), amino acids ( glutamate, GABA, glycine), biogenic amines ( dopamine, norepi, and epi)

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3
Q

what is special about the amino acid neurotransmitters, glutamate, GABAand glycine?

A

they are in every synapse glutamate is excitatory, and GABA and glycine are inhibitory

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4
Q

what are peptide neurotransmitters important for?

A

transmission and blocking of pain.

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5
Q

what does removal of neurotransmitters from the synapse do?

A

terminate synaptic transmission

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6
Q

the concentration of neurotransmitter w/in the synaptic cleft is tightly controlled via regulation of what 4 processes?

A

neurotransmitter synthesis, packaging, release and removal

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7
Q

where are neuropeptide neurotransmitters made?

A

in the ER

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8
Q

where are small molecule neurotransmitters made?

A

in the presynaptic terminal

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9
Q

ligand gated ion channels are?

A

ionotropic

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10
Q

G-prootein coupled channels are?

A

metabotropic

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11
Q

Metabotropic neurotransmitters are ___________ than ionotropic transmitters

A

slower

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12
Q

1 alpha and 1 beta are required to be what type of receptor?

A

GABA

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13
Q

iontoropic receptors have how many subunits that contain how many transmembrane domains?

A

iontoropic receptors are usually 4-5 subunits that contain 3 or 4 transmembrane domains

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14
Q

metabotropic receptors have how many transmembrane domains?

A

7

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15
Q

what are the major biogenic amine neurotransmitters?

A

dopamine, norepinephrine, serotonin

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16
Q

what is the major neurotransmitter in the neuromuscular junction of the peripheral nervous system and where else is it the major neurotransmitter?

A

acetylcholine which is also the major neurotransmitter in the parasympathetics

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17
Q

where is acetylcholine synapse in the peripheral nervous system?

A

in the ganglia of the visceral motor sys

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18
Q

what are the fmcs of Ach in the CNS?

A

attention, arousal, reward plasticity, enhances sensory fnc upon waking

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19
Q

what is damage to the Ach sys ( cholinergic sys) in the CNS associated w/?

A

memory deficits in alzheimer’s

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20
Q

what does acetylcholinesterase do?

A

it cleaves acetylcholine to acetate and choline ( this occurs in the synaptic cleft in the CNS and in the basal lamina in the periphery

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21
Q

where is achetocholine degraded?

A

in the synaptic cleft

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22
Q

sarin gas and other nerve gases and insecticides which inhibit acetylcholinesterase do what?

A

cause Sch to accumulate resulting in continued depolarization of the postsynaptic cell and leads to muscle paralysis at the neuromuscular junction.

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23
Q

are acetylcholine receptors ionotropic or metabotropic?

A

there are both metabotropic (muscarinic)and ionotropic (nicotinic) Ach receptors

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24
Q

where do ionotropic (nicotinic) acetylcholine receptors act?

A

in the periphery in the neuromuscular junction and also in the CNS

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25
Q

where do metabotropic ( muscarininc) receptors act?

A

they mediate most Ach effects in the brain

and they are involved in autonomic effector organs in the heart, smooth muscle etc.

26
Q

name 2 metabotropic Ach receptor antagonists.

A

atropine ( cause pupil dialation)

scopolamine ( motion sickness)

27
Q

what is myasthenia gravis?

A

an autoimmune disease in which pts have antibodies against the muscle nicotic ( ionotropic) Ach Receptor leading to decreased receptors in the postsynaptic membrane, expanded synaptic cleft, and shallow junctional folds ( see pg 145)

28
Q

what are the symptoms of myasthenia gravis?

A

weakness, fatiguability in the arms and legs, difficulty speaking and swallowing, chewing , diplopia, and ptosis

29
Q

how do you treat myasthenia gravis?

A

by giving CHOLINESTERASE INHIBITORS to prevent the sparse number of Ach receptors the pt has from breaking down.

or THYMECTOMY surgically remove the thymus

or CORTICOSTEROIDS

or IMMUNOSURPRESSANTS - to decrease the autoimmune response to AchRs

30
Q

What is the most prominent transmitter for normal brain fnc (CNS)?

A

glutamate

31
Q

and in crease in extracellular glutamate can lead to ?

A

excitotoxicity causing neurons to over excite and die

32
Q

excitotoxicity of glutamate is seen in which medical problems or disease?

A

strokes, hypoglycemia, trauma, and repeated intense seizures

33
Q

can glutamate cross the blood brain barrier?

A

no but glutamine can

34
Q

what happens to glutamate in glial cells?

A

they are converted to glutamine ( for transport out of cells) which prevents the excitotoxicity from occurring

35
Q

what are 3 types of glutamate receptors?

A

NMDA, AMPA and Kainate

36
Q

what are 3 unique properties of NMDA compared to the other glutamate receptors?

A
  • ca2+ can pass through it
  • ion flow is voltage dependent because of the Mg2+ binding
  • glycine binding is required to the open channel
37
Q

where is GABA used in the CNS

A

in 1/3 of brain synapse , used in interneurons and purkinje fibers of the cerebellum

38
Q

where is glycine used in the CNS?

A

at synapses in the spinal cord.

39
Q

decreased GABA function can cause?

A

epilepsy

40
Q

excess glycine can cause ?

A

neonatal disease characterized by lethargy and mental retardation.

41
Q

glycine is made in nerve terminals from?

A

serine

42
Q

GABA is made in nerve terminals from?

A

glutamate

43
Q

where is glutamate made and used in the brain?

A

all over the place ( everywhere)

44
Q

what are GABA receptor agonists used for?

A

they are tranquilizers and control epilepsy and can be used to treat panic disorders and anxiety.

45
Q

what is an example of aGABA antagonists?

A

strychnine ( used in rat poison) it causes overactivity in spinal cord and brain stem leading to seizures

46
Q

where are biogenic amines synthesized in the brain compared to GABA?

A

the amines are synthesized in specific layers but their receptors are more broadly distributed.

47
Q

are biogenic amines released and removed from nerve terminals by the same means or different means?

A

by the same means ( they are les reliant on glial cells)

48
Q

are biogenic amines greatly used in the brain?

A

they are used by relatively few neurons in the brain but they are very important in maintenance of mental health

49
Q

a dopamine input to the corpus striatum is seen in what disease?

A

parkinson’s disease

50
Q

cocaine interferes with the reuptake of what receptors?

A

dopamine receptors, therefore it raises dopamine levels

51
Q

what is the major fnc of dopamine?

A

involved in ovation, reward and reinforcement ( this takes place in the midbrain dopamine system)

52
Q

what is the minor dopamine fnc?

A

it is involved in emotional behavior ( localization of this involvement: in the projections to the cortex)

53
Q

dopamine receptors act by?

A

activating or inhibiting adenlyl cyclase

54
Q

why are ppl on amphetamines hyped up?

A

because it inhibits dopamine and norepi transporters causing an increase in release of them.

55
Q

although it is hard to clinically distinguish norepi and serotonin how are they different?

A

norepi is mood activating

serotonin is mood altering

56
Q

what is the dopamine hypothesis?

A

that too much dopamine leads to psychosis

57
Q

what do anti-psychotic drugs block?

A

drugs block dopamine receptors

58
Q

what do anti- anxiety drugs (MAO inhibitors and _________)?

A

block the breakdown of biogenic amines and therefore increase biogenic amines

and inhibitors of serotonin receptors

59
Q

what are the 3 classes of anti depressants include?

A

MAO inhibitors ( biogenic amine receptor breakdown)

tricyclic anti-depressants ( block reuptake of Norepi)

serotonin reuptake inhibiotrs ( like prozac)

60
Q

how are peptide neurotransmitters removed from the synaptic cleft ?

A

via degradation by peptidases

61
Q

see chart on 165

A

see chart

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