Chapter 6: Neurotransmitters and their receptors Flashcards

1
Q

how big are neuropeptides?

A

3 to 36 amino acids (large neurotransmitters)

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2
Q

small-molecule peptides (individual amino acids or transmitters) include…

A

glutamate, GABA, acetylcholine, serotonin, and histamine

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3
Q

give examples of biogenic amines (sub category of small-molecule peptides grouped due to their similar chemical properties and postsynaptic actions)

A

dopamine, norepinephrine, epinephrine, serotonin, and histamine

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4
Q

what is the role of ACh?

A

it is the neurotransmitter at skeletal
neuromuscular junctions, as well as at the neuromuscular synapse between the vagus nerve and cardiac muscle fibres.

ACh also serves as a transmitter at synapses in the ganglia of the visceral motor system and at a variety of sites in the CNS

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5
Q

what is acetylcholinesterase (AChE)?

A

a powerful hydrolytic enzyme that reuptakes ACh from cholinergic synapses (particularly the NMJ).

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6
Q

the nerve gas sarin is an example of what?

A

an organophosphate (a drug that interacts with cholinergic enzymes)

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7
Q

how are organophosphates lethal?

A
  • They inhibit AChE, allowing ACh to accumulate at cholinergic synapses.
  • This build-up of ACh depolarizes the
    postsynaptic muscle cell and renders it refractory to subsequent ACh release, causing neuromuscular paralysis and
    other effects
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8
Q

Many of the postsynaptic actions of ACh are mediated by which receptor?

A

the nicotinic ACh receptor (nAChR) (ionotropic ligand-gated ion channel)

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9
Q

what are muscarinic ACh receptors (mAChR)?

A

mAChRs are metabotropic and mediate most of the effects of ACh in the brain

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10
Q

name all the types of metabotropic neurotransmitter receptors (8)

A
  1. muscarinic
  2. glutamatergic
  3. GABAb
  4. dopamine
  5. adrenergic
  6. histamine
  7. serotonin
  8. purine
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11
Q

mAChR blockers that are therapeutically useful include atropine, scopolamine and ipratropium. what do they do?

A

atropine (used to dilate the
pupil)
scopolamine (effective in preventing motion sickness)
ipratropium (useful in the treatment of asthma

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12
Q

what is involved in the glutamate–glutamine cycle? (3)

A
  • Glutamate synthesized in the presynaptic cytoplasm is packaged into synaptic vesicles
    by vesicular glutamate transporters (VGLUTs).
  • Once released, glutamate is removed from the synaptic cleft by the excitatory amino acid transporters (EAATs).
  • Glutamine is then transported out of the glial cells by a different transporter, the system N transporter 1 (SN1), and transported into nerve terminals via SAT2.
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13
Q

which type of glutamatergic receptor are the primary mediators of excitatory transmission in the brain?

A

AMPARs

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14
Q

what is a difference between excitatory ionotropic glutamate receptors and metabotropic glutamate receptors?

A

mGluRs cause slower postsynaptic responses that can either excite or inhibit postsynaptic cells.

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15
Q

how is the structure of mGluRs unique?

A

they are dimers of two identical subunits

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16
Q

why did lack of vitamin B6 in infant formula cause a series of infant deaths?

A
  • GAD catalyzes the conversion of glutamate to GABA
  • GAD requires a co-factor, pyridoxal phosphate, for activity.
  • Because pyridoxal phosphate is derived from vitamin B6, a deficiency of this vitamin can lead to diminished GABA synthesis.
  • the subsequent loss of synaptic inhibition caused seizures that in some cases were fatal
17
Q

biogenic amines are implicated in which behaviours?

A

ranging from central homeostatic functions to cognitive phenomena such as attention

18
Q

what are the five well-established biogenic amine neurotransmitters?

A

the three catecholamines dopamine,
norepinephrine (noradrenaline), and epinephrine (adrenaline),
and histamine and serotonin

19
Q

how does cocaine exert its psychotropic effects?

A

by inhibiting DAT, thereby increasing dopamine concentrations in the synaptic cleft