E3 Amino Acid Neurotransmitters Flashcards

1
Q

T/F: amino acid neurotransmitters are the most prevalent neurotransmitter in the CNS

A

true

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2
Q

what are the two major classes of amino acid neurotransmitters?

A

excitatory amino acid and inhibitory amino acids

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3
Q

what are the two excitatory amino acids?

A

glutamate and aspartate

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4
Q

what are the two inhibitory amino acids?

A

GABA and glycine

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5
Q

Is glutamate ionotropic or metabotropic?

A

mostly ionotropic but have some degree of metabotropic binding?

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6
Q

What does ionotropic mean?

A

membrane-bound receptor proteins that respond to ligand binding by opening an ion channel and allowing ions to flow into the cell

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7
Q

what does metabotropic mean?

A

indirectly linked with ion channels on the plasma membrane of the cell through signal transduction mechanisms (g-protein)

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8
Q

what are the two receptors associated with glutamate?

A

AMPA and NMDA

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9
Q

what is NMDA associated with?

A

excitotoxicity (overproduction can cause neuronal damage)

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10
Q

what does the cooperation of AMPA and NMDA receptors lead to?

A

long-term potentiation (long-term synaptic plasticity)

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11
Q

what is long-term synaptic plasticity associated with?

A

long-term learning

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12
Q

what does frequent activity across a synapse cause?

A

lasting changes in strength of signaling (enhancement of neuroplasticity)

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13
Q

What is neuroplasticity?

A

the ability of the nervous system to change in response to experience or the environment

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14
Q

In the activation of glutamate receptors, what does AMPA require to open its ion channel?

A

the binding of glutamate

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15
Q

what does the activation of AMPA lead to?

A

membrane depolarization and excitatory transmission

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16
Q

In the activation of glutamate receptors, what needs to bind to NMDA?

A

both glutamate and glycine (they bind to diff. sites)

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17
Q

what is the ion channel of NMDA blocked by?

A

Magnesium

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18
Q

what displaces the magnesium cork from NMDA?

A

depolarization by the activation of AMPA receptor displaces the magnesium cork

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19
Q

what occurs when the magnesium cork is displaced from NMDA

A

-opening of NMDA ion channel
-Ca2+ influx (contributes to long-term potentiation)

20
Q

can glutamate pas through the BBB?

A

no - must be synthesized in the brain

21
Q

what is glutamate synthesized from

A

alpha ketogluterate

22
Q

what does glutamates interaction with the excitatory receptors cause?

A

a greater chance that an action potential will be fired

23
Q

how does glutamate increase the change of an action potential being fired?

A

when glutamate binds to the receptors and the ion channels open the influx of Na+ causes depolarization

24
Q

what are the metabotropic effects of glutamate?

A

glutamate is removed from the synaptic cleft by exciatory amino acid transporters (EAATS)

25
Q

What do EAATs do?

A

carry glutamate into glial cells

26
Q

what occurs to glutamate in the glial cells?

A

-converted to glutamine by glutamine synthetase

27
Q

what occurs to glutamate after it has been converted to glutamine?

A

transporter back into neurons where it is converted back into glutamine

28
Q

what is the process of converting glutamate into glutamine back into glutamate called?

A

glutamate/glutamine cycle

29
Q

what are the steps of glutamate receptor activation?

A
  1. action potential into presynaptic cell
  2. glutamate release (Ca2+ mediated exocytosis)
  3. glutamate binds to both channels
  4. Na+ influx (depolarization)
  5. depolarization drives Mg2+ ion out of pore
  6. Ca2+ activates 2nd messenger system
  7. long-lasting increase in glutamate receptors and sensitivity
30
Q

what are the two inhibitory amino acids?

A

GABA and glycine

31
Q

what is GABA modified from?

A

glutamate (decarboxlyzed from glutamate to GABA)

32
Q

where is GABA located?

A

interneurons that dampen circuits (synapses in CNS)

33
Q

What forms of GABA are ionotropic?

A

GABA(A) and GABA(C)

34
Q

what is the direct ionotropic effect of GABA

A

GABA binds to the receptors on a neuron and causes the opening of Cl- channels (hyperpolarization)

35
Q

what is the indirect ionotropic effect of GABA?

A

opening of K+ channels or blocking of Ca2+

36
Q

what form of GABA is metabotropic?

A

GABA(B) - g-protein linked (open close channels via intermediates)

37
Q

what are the metabotropic effects of GABA

A

-indirect g-protein linked opening of K+ channels or blocking of Ca2+ channels

38
Q

what occurs when GABA interacts with receptors of a neuron?

A

makes the neuron less likely to fire and action potential or release neurotransmitters

39
Q

how is GABA terminated

A

GABA transporters transport GABA from synaptic cleft into neurons or glial cells where it is degraded by mitochondrial enzymes

40
Q

what does increased GABA activity cause?

A

sedative effects

41
Q

what increases the activity of the GABA receptor?

A

alcohol and benzodiazepines

42
Q

Where is glycine located?

A

spinal cord and brain stem (not in cerebral hemispheres)

43
Q

is glycine ionotropic or metobotropic?

A

ionotropic (chloride influx)

44
Q

what is glycine synthesized from?

A

serine

45
Q

how is glycine synthesized?

A

serine-hydroymethyltransferase converts serine to glycine

46
Q

what is the vesicular GABA transporter used for in glycine inhibition?

A

glycine is transported into vesicles where it is stored

47
Q

what are the steps of the glycine inhibitory pathway?

A
  1. Ca2+ enters the presynaptic cell
  2. Ca 2+ mediated exocytosis of glycine
  3. glycine binds to ligand-gated Cl- receptor
  4. influx of Cl- causes hyperpolarization
  5. glycine is removed from synapse through the glycine reuptake channel and recycled