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PSYC 462 > CH. 8 Glutamate > Flashcards

CH. 8 Glutamate Flashcards

1
Q

what is glutamates function?

A

basis of all signalling

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2
Q

projection neurons that use glutamate

A

cortex pyramidal cells
hippocampus, amygdala, thalamus
other subcortical nuclei

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3
Q

what are the roles glutamate can play?

A

neurotransmitter
metabolic

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4
Q

how do other neurotransmitters affect glutamate

A

modulate effects

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5
Q

true or false; some neurons only use ‘classical’ NTs over glutamate

A

false; glutamate is necessary for signalling

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6
Q

amino acid that glutamate ionizes from

A

glutamic acid

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7
Q

precursor to glutamate

A

glutamine

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8
Q

enzyme that synthesizes glutamate from glutamine

A

glutaminase

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9
Q

how can you tell if glutmate is being used as a transmitter instead of another one of its functions?

A

glutamate as an NT is transported in vesicles

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10
Q

what are glutmates vesicular transporters called?

A

VGLUT

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11
Q

what is a good marker for glutamatergic neurons?

A

VGLUT transporters

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12
Q

what type of VGLUT transporters are there?

A

VGLUT1
VGLUT2
VLGUT3

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13
Q

what happens when VGLUT knockout occurs? what does this indicate to us?

A

fatality
necessary for life in all stages

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14
Q

how does glutamate interact with other NTs?

A

can be a co-transmitter with the ‘primary’ transmitter

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15
Q

what is a way an axon with multiple NTs can organize

A

separate terminals for separate NTs

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16
Q

name of the transporters that remove glutamate from the synapse after release

A

EAAT

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17
Q

what does EAAT stand for

A

Excitatory Amino Acid Transporter

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18
Q

what are the different kinds of reuptake transporters

A

EAAT1 to EAAT5

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19
Q

where are EAAT1-2 transporters found

A

astrocyte glia

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20
Q

which glutamate transporters do the most reuptake?

A

1 and 2 (astorcyte)

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21
Q

where are EAAT3 reuptake transporters found?

A

postsynapse

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22
Q

what happens to glutamate after astrocyte reuptake?

A

converted to inactive glutamine

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23
Q

what enzyme converts glutamate to glutamine?

A

glutamine synthetase

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24
Q

what is a reason glutamate is converted to its inactive form when reuptaken?

A

any possible leak will only leak inactive glutamine

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25
Q

what happens when glutamate is released in the synapse?

A

excites

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26
Q

what happens when excitation does not turn off in a neuron

A

excitoxic effects; kills the neuron

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27
Q

what is a consequence of glutamate’s excitatory effects?

A

very tightly regulated

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28
Q

what happens with glutamine in the glia

A

transported back to the presynaptic terminal
can be reactivated here

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29
Q

how can glutamate function as a method in neuroscience studies?

A

used to make excitotoxic lesions

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30
Q

what kind of receptors does glutamate have?

A

ionotropic
metobotropic

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31
Q

what are the different kinds of ionotropic glutamate receptors

A

AMPA
Kainate
NMDA

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32
Q

what is the basis of naming receptors

A

named after the drug that activated them (agonists)

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33
Q

how are the ionotropic glutamate receptors structured

A

4 protein subunits
have subsubunits that vary based on function/area
center is ion pore

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34
Q

what do non-NMDA receptors do when activated

A

depolarizes neuron by allowing entry of NA+

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35
Q

how can non-NMDA receptors sensitivity to glutamate be regulated?

A

affinity change
removed from membrane
shorter/longer activation period

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36
Q

what causes a non-NMDA receptor to desensitize?

A

too much stimulation

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37
Q

true or false; sensitization and desensitization occur quickly in neurons like a conveyor belt

A

true

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38
Q

Kynurgic acid drug function

A

non-selective/broad spectrum antagonist to AMPA, Kainate, and NMDA receptors

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39
Q

NBQX drug function

A

competitive antagonist blocks non-NMDA receptors

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40
Q

side effects of high dose NBQX

A

sedation
reduced locomotion
ataxia

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41
Q

what drug can be used to treat against seizures?

A

NBQX

42
Q

what exactly is a seizure

A

large group of neuronsfiring at the same time instead of in patterns; excitotoxicity occurs

43
Q

what do NMDA receptor do when activated

A

allow flow of Na+ and Ca+2 into neuron

44
Q

what differences does the inflow of Ca+2 in NMDA receptors cause?

A

greater depolarization
activation of other enzymes leading to longer term changes

45
Q

what are the coagonists for NMDA receptors

A

glycine or D-serine

46
Q

what binding sites can be found on NMDA receptors

A

glutamate binding site
coagonist binding site

47
Q

what needs to happen for NMDA receptors to activate

A

Glutamate binding
coagonist binding
removal of Mg+2 block in pore

48
Q

what needs to happen to dislodge the Mg+2 block in the NMDA receptor? what does this mean?

A

membrane depolarization
NMDA is voltage dependent and neuron must already be depoalrized before they activate

49
Q

what depolarizes NMDA receptors enough for them to activate

A

multiple AMPA receptor activation

50
Q

competitive antagonist drug of NMDA receptors

A

AP-5

51
Q

what does AP-5 do

A

blocks glutamate from binding to NMDA receptor

52
Q

what do non-competitive antagonists do to NMDA receptors

A

block receptor at a spot other than the glutamate binding area

53
Q

drugs that block NMDA channel

A

Phencyclidine (PCP)
ketamine
MK-801

54
Q

what do non-competitive agonists drugs do at low doses

A

cause schizophrenia-like symptoms

55
Q

what do pore plug antaogist drugs do at high doses

A

cause ataxia and anesthesia

56
Q

what is a way that a drug can act as a positive allosteric modulator on the NMDA receptor?

A

increasing affinity or efficacy of the receptor when bound to the coagonist binding site

57
Q

what are the differences in excitatory effects between AMPA/Kainate and NMDA?

A

AMPA; high and fast peak activation and degrades quickly
NMDA; shorter peak of activation but longer change in depolarization. alters firing patterns (promotes burst firing)

58
Q

how are the different effects of ionotropic glutamate receptors measured?

A

patch clamp recordings of isolated AMPA or NMDA activation

59
Q

how many metabotropic glutamate receptors are there and what are they called

A

8, mGluR

60
Q

where are mGluR 1 and 5 found

A

postsynapse

61
Q

where are mGluR 2-4 and 6-8 found?

A

presynapse

62
Q

what are the functions of the presynaptic mGluR

A

surpress glutamate release as autoreceptors or heteroreceptors

63
Q

L-AP4 drug function

A

agonist of mGluR 4/6/7/8 autoreceptors

64
Q

what brain functions do mGluRs participate in

A

widely distributed
locomotion
motor coordination
cognition
mood and pain perception

65
Q

what is the most studied function of glutamate receptors

A

synaptic plasticity for learning/memory

66
Q

how can we measure alterations in the activity of synapse

A

measuring changes in synaptic strength

67
Q

how do we measure synaptic strength

A

changes in post synaptic potential measured with electrophysiological methods
larger EPSP is higher strength

68
Q

what does LTP stand for?

A

long-term potentiation

69
Q

what is LTP?

A

model of underlying formation of memory

70
Q

what are the steps of an experiment that showed LTP? what were the results?

A
  1. measure the subthreshold EPSP of a cell with a low frequency stimulation to establish the baseline
  2. stimulate cell with high frequency
  3. stimulate with low frequency subthreshold current again

vigourous activation causes baseline EPSP to increase long-term in strength and therefore male it more likely to cause AP

71
Q

how does LTP work in general on our memories?

A

initial experience; group of neurons fire in a certain pattern
recalling the experience; group of neurons fire in the same pattern of the original experience

72
Q

phases of LTP

A

early phase
late phase

73
Q

steps of early phase LTP

A

high frequency activates NMDA receptor and Ca+2 enters post synapse
Ca+2 activates kinases including CaM kinase

74
Q

what are the results of early phase LTP

A

CaM kinase takes extra AMPA receptors and puts them in the membrane
other kinases induce formation of retrogade messenger
dendritic spine structure changes to make them more excitable
synaptic strength increases

75
Q

what does the retrograde messenger do?

A

sends NO to the pre-synapse that facilitates more NT release

76
Q

how does CaM change AMPA receptors chemically

A

adds phosphorous to them which gives them a higher affinity for the membrane

77
Q

what is the structural change that occurs in the post synapse?

A

spines get thicker

78
Q

what happens in late phase LTP?

A

same as early phase, but synthesizes proteins that make the changes last longer

79
Q

how does late phase LTP trigger the synthesis of new proteins?

A

cell nucleus DNA activation is changed to make different proteins

80
Q

what happens if you block NMDA receptors

A

cannot do LTP

81
Q

what happened to rats placed in the MWM that had NMDA receptors blocked

A

control rats used cues to find platform and got quicker with more trials
NMDA antagonist rats showed no increased efficiency to finding the platform

82
Q

what happens with glutamate activity increase?

A

slightly improves learning

83
Q

what happens if you block AMPA receptors

A

cells cannot function correctly

84
Q

what are ampakines? what do they do?

A

positive allosteric modulators of AMPA receptors
prolong open time and reduce desensitization

85
Q

what was found in monkey study when using ampakines

A

higher doses of ampakines improved cognitive task of matching objects

86
Q

what happens when glutamate activity is highly increased?

A

excitotoxicity

87
Q

what is excitotoxicity? what are the different types?

A

prolonged depolarization of neurons that leads to damage or death
necrosis, apoptosis

88
Q

what is necrosis?

A

fast death of cells

89
Q

what happens during necrosis

A

ion channels stay activated
too many ions enter the cell
cell swells
death by lysis

90
Q

what is lysis

A

bursting of cells due to ruptures in the cell membrane

91
Q

what is another name for apoptosis?

A

programmed necrosis

92
Q

what is apoptosis

A

slow cell death through biochemical events

93
Q

what causes apoptosis

A

long exposure to low concentrations of ions
Ca+ trigger ‘death’ enzymes instead of regular ones when the cell gets too much

94
Q

what kind of excitotoxicity depends on NMDA receptor activation?

A

apoptosis

95
Q

true of false; lysis occurs in necrosis and apoptosis

A

false; lysis does not occur in apoptosis

96
Q

what is a natural cause of excitotoxicity

A

brain ischemia

97
Q

what is a brain ischemia

A

interuption of blood flow to the brain because of a stroke/heart attack

98
Q

why does a brain ischemia cause excitotoxicity

A

blood cannot reach brain
oxygen is not coming to the brain
K+/ Na+ pump does not function
cell depolarizes
cell cannot reset properly and calcium builds up
calcium build up triggers ‘death’ enzymes

99
Q

how do NMDA antagonists work against brain ischemia effects?

A

they don’t
if already in apoxic state, killer enzymes have already been triggered and will continue to kill cells days afterwards

100
Q

why is it not plausible to administer drugs that will deactivate killer enzymes

A

they may have affinity for other enzymes necessary for proper function

PSYC 462 (11 decks)

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