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OPT 112 > Neurotransmitters (M2) > Flashcards

Neurotransmitters (M2) Flashcards

1
Q

when is acetylcholine (ACh) utilized

A

in synapses within the cns and pns

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2
Q

cholinergic neurons

A

neurons that utilize ACh as the primary neurotransmitter

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3
Q

cholinergic synapse

A

synapse employing ACh

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4
Q

choline acetyl transferase (ChAT)

A

enzyme that synthesizes ACh within the synaptic vesicle of the presynaptic cell

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5
Q

what is acetyl CoA formed from

A

acetate and coenzyme A (CoA) by a synthetase enzyme

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6
Q

what does botulinum toxin bind to

A

SNARE proteins, which prevents vesicles from releasing excitatory ACh

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7
Q

acetylcholinesterase (AChE)

A

enzyme that does enzyme degradation of ACh in the synaptic cleft

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8
Q

4 processes involved in removing neurotransmitters from the synaptic cleft

A
  1. reuptake of NT into the presynaptic cell via active transport and repackaged into vesicles
  2. uptake of NT by surrounding glial cells
  3. diffusion of NT away from synaptic cleft
  4. enzymatic degradation of NT (ex. acetylcholinesterase)
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9
Q

what does ACh bind to within the cholinergic synapse

A

nicotinic (nicotine-binding) or muscarinic (muscarine-binding) receptors of the postsynaptic cell

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10
Q

are nicotinic receptors ionotropic or metabotropic? excitatory or inhibitory?

A

ionotropic
excitatory

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11
Q

are muscarinic receptors ionotropic or metabotropic? excitatory or inhibitory?

A

metabotropic
excitatory or inhibitory

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12
Q

location of nicotinic receptors

A

somatic effectors (skeletal muscle) at neuromuscular junctions within somatic nervous system.
ganglionic neurons at their synapse with preganglionic neurons in the autonomic ganglia of the ANS.
chromaffin cells of the adrenal medulla.
in postsynaptic cells within spinal cord gray matter of cns

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13
Q

location of muscarinic receptors

A

autonomic effectors (cardiac and smooth muscle, glands except sweat) at its synapse with parasympathetic ganglionic neuron (postg.) in ans.
autonomic effectors (sweat glands) at its synapse with sympathetic ganglionic neuron (postg.) in ans.
postsynaptic cells within gray matter in various areas of the brain of the cns.

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14
Q

ACh and alzheimer’s

A

neurons associated with ACh system degenerate in people with Alzheimer’s.
decreased amount of ACh in certain areas of the brain and even the loss of the postsynaptic neurons that would have responded to it.
these defects are related to the declining language and perceptual abilities, confusion, and memory loss that characterize alzheimer’s victims.

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15
Q

structure of catecholamines

A

6-carbon ring with 2 hydroxyl groups (catechol) plus an amine group and formed by uptake of amino acid, tyrosine, into axon terminal

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16
Q

what originates from tyrosine

A

dopamine
norepinephrine (noradrenaline)
epinephrine (adrenaline)

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17
Q

where are cell-bodies of catecholamine-releasing neurons located

A

within hypothalamus and brainstem of cns.
- few in number, but the axons of these neurons branch significantly and project to virtually all areas of the brain and spinal cord.

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18
Q

what do catecholamines exert

A

essential functions on consciousness, mood, attention and movement, blood pressure, and hormone release

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19
Q

where are epinephrine and norepinephrine synthesized besides its synthesis in axon terminals

A

medulla of adrenal gland –> also classified as hormones

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20
Q

monoamine oxidase (MAO)

A

enzyme that degrade catecholamines

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21
Q

MAO inhibitors

A

increase amount of dopamine and norepinephrine by slowing their degradation

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22
Q

what does dopamine bind to

A

dopaminergic receptors (metabotropic)

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23
Q

where are dopaminergic receptors found

A

mostly in the cns.
present to a lesser degree in the pns.

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24
Q

does dopamine act as a neurotransmitter or hormone

A

can act as a neurotransmitter or travel through the blood and act on other cells as a hormone

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25
Q

effects of dopamine

A

reward and motivation.
blood pressure and fluid regulator.
affects secretion of other hormones.

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26
Q

where are adrenergic receptors found

A

located on autonomic effectors (cardiac and smooth muscle, glands) at its synapse with the sympathetic ganglionic neuron (postg.) in the ans

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27
Q

what do adrenergic receptors bind

A

catecholamine neurotransmitters norepinephrine and epinephrine

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28
Q

are adrenergic receptors metabotropic or ionotropic? exert excitatory or inhibitory effects?

A

metabotropic.
exert excitatory or inhibitory effects on postsynaptic cell.
second messenger pathways can vary by adrenergic receptor type.

29
Q

what are the adrenergic receptors

A

alpha-adrenergic receptors: alpha1 and alpha2.
beta-adrenergic receptors: beta1, beta2, beta3.

30
Q

norepinephrine effects on adrenergic receptors

A

can work on alpha-adrenergic and beta-adrenergic receptors.
impacts on beta-adrenergic receptors are not as robust as with epinephrine

31
Q

epinephrine effects on adrenergic receptors

A

can work on alpha-adrenergic and beta-adrenergic, but more robust response when bound to beta-adrenergic than norepinephrine

32
Q

what are indolamines

A

second subclass of the biogenic amine neurotransmitters

33
Q

what is the structure of serotonin and location

A

5-hydroxytryptamine or 5-HT.
found in vast majority of brain and spinal cord structures (CNS) and derived from amino acid tryptophan.
also made by enterochromaffin cells in the gut and taken up and stored in nerve terminals and platelets.

34
Q

what does serotonin exert excitatory and inhibitory effects on

A

exerts excitatory effect muscle control and inhibitory effect on pathways that mediate sensation.
levels lowest during sleep and highest during alterness

35
Q

what are SRIs

A

serotonin reuptake inhibitors.
believed to aid in management of depression (ex. paroxetine = Paxil).

36
Q

what is histamine misclassified as

A

indolamine.
it is a biogenic amine - derived from the amino acid histidine, which does not have an indole group in its chemical structure.

37
Q

main cns location of serotonin

A

brainstem

38
Q

functions of serotonin

A

regulating sleep.
emotions (obsessions, compulsions).
memory.
appetite/weight changes.
5-HT3 receptors in the medulla of the brainstem (‘area postrema’) are involved in vomiting reflex.
regulates cell growth.
vascular smooth muscle cell contraction.

39
Q

general knowledge about parkinson’s disease

A

involves the loss of dopamine-releasing neurons in the substantia nigra of the midbrain which affects motor contol.
cause of disease is not clearly understood, loss of dopamine neurons is critical.

40
Q

symptoms of parkinson’s disease

A

persistent tremors.
head nodding and pill rolling behaviors.
forward bent walking posture.
shuffling gait.
still facial expressions.
slow in initiating and executing movement.

41
Q

what are symptoms of parkinson’s disease managed with

A

the drug L-Dopa (precursor to dopamine) in the initial stages to alleviate symptoms and often concomitantly prescribed with the drug deprenyl (prevents L-Dopa degradation)

42
Q

experimental treatments for parkinson’s

A

deep brain stimulation by surgically implanting electrodes, and gene therapy

43
Q

qualities and examples of amino acids that act as neurotransmitters

A

short-acting.
glutamate.
aspartate.
glycine

44
Q

what is glutamate and where is it found

A

primary neurotransmitter at 50% of the excitatory synapses in the cns.
most common in cns; synthesized in mitochondria from glucose and glutamine

45
Q

types of glutamate receptors

A

ionotropic glutamate receptors: very active and one of the major cellular processes in learning and memory.
- AMPA receptors (bind to alpha-amino-3-hydroxy-5-methyl-4 isoxazolepropionic acid).
- NMDA receptors (bind N-methyl-D-aspartate).
Metabotropic glutamate receptors

46
Q

qualities of AMPA ionotropic glutamate receptors

A

fast EPSP.
conduction of Na+.

47
Q

qualities of NMDA ionotropic glutamate receptors

A

at resting membrane potential, NMDA channels are blocked by Mg2+.
AMPA receptor EPSPs change membrane potential by 20-30 mV is enough to bump Mg2+ from NMDA channel, allowing for influx of Ca2+.
Important in exocytoxicity.

48
Q

what is glutamate recycled by and what happens

A

recycled by glial cells and converted into glutamine for reuptake by presynaptic cell

49
Q

what is GABA

A

gamma-aminobutyric acid.
most common inhibitory neurotransmitter - dampens neural activity in the brain.
derived from an enzymatically-modified form of glutamate.

50
Q

what does GABA bind to and what happens

A

binds to ion channels and cause immediate change in membrane potential to a more negative charge as Cl- channels are open

51
Q

what do GABA receptors possess

A

additional binding sites that serve as targets for steroids, ethanol, and drugs including barbiturates and benzodiazepines (Xanax, Valium)

52
Q

what are GABA receptors

A

GABA sub A (ionotropic).
GABA sub B (metabotropic)

53
Q

what is glycine converted by and what is it

A

converted from serine by an enzyme.
inhibitory neurotransmitter of the brainstem and spinal cord.

54
Q

how does glycine cause an IPSP

A

increases Cl- influx into the postsynaptic cell like GABA.

55
Q

why is glycine important

A

acts on spinal integration centers of the spinal cord that regulate skeletal muscle contraction

56
Q

what is strychnine

A

glycine antagonist.
causes hyperexcitability through the nervous system leading to convulsions and spastic contraction of skeletal muscles (spastic paralysis)

57
Q

what are neuropeptides

A

amino acid chain.
maybe made as a precursor molecule.
stored in dense core vesicles.
modulate responses.
growth factors, hormones

58
Q

why is nitric oxide different from the classic neurotransmitters

A

not stored in vesicles.
synthesized on an ‘as needed’ basis in the postganglionic neurons and released from these cells that can act on preganglionic neurons (retrograde) to release additional neurotransmitters

59
Q

what happens to nitric oxide in the postsynaptic cell

A

synthesized from the amino acid arginine in a Ca2+/calmodulin-dependent manner and catalyzed by the enzyme NO synthase

60
Q

what does nitric oxide activate

A

cGMP - second messenger

61
Q

functions of nitric oxide

A

vasodilation.
long-term potentiation (memory).

62
Q

what is too much nitric oxide

A

proinflammatory and can be cytotoxic

63
Q

nitric oxide isoforms

A

nNOS
eNOS
iNOS

64
Q

what are the metabolically active molecules

A

carbon monoxide (CO).
hydrogen sulfide (HS).
purines: ATP and adenosine

65
Q

what are endocannabinoids synthesized and released from

A

postsynaptic cells

66
Q

what do endocannabinoids do

A

decrease neurotransmitter release from presynaptic neurons.
alter memory and cognition.
increase appetite.

67
Q

what are anandamide (AEA) and 2-arachidonoyl-glycerol (2-AG) and what do they bind to

A

endocannabinoids.
bind to CB1 and CB2 cannabinoid receptors.

68
Q

what is tetrahydrocannabinol and what does it bind to

A

active ingredient in marijuana.
can bind to CB1 and CB2 receptors.

69
Q

what can a drug do

A
  1. increase leakage of neurotransmitter from vesicle to cytoplasm, exposing it to enzyme breakdown.
  2. increase transmitter release into cleft.
  3. block transmitter release.
  4. inhibit transmitter release.
  5. block transmitter reuptake.
  6. block cleft enzymes that metabolize transmitter.
  7. bind to receptor on postsynaptic membrane to block (antagonist) or mimic (agonist) transmitter action.
  8. inhibit or stimulate second-messenger activity within postsynaptic cell.

OPT 112 (9 decks)

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