Karius- EAA System & Excitotoxicity Flashcards

1
Q

2 main EAAs?

A

glutamate and aspartate

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2
Q

where is aspartate used as NT?

A

visual cortex and pyramidal cells

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3
Q

what are the ionotropic EAA receptors?

A

NMDA and non-NMDA

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4
Q

what do NMDA receptors allow in?

A

Calcium

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5
Q

what is required as a co-agonist for glutamate on NMDA?

A

glycine

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6
Q

What are the 2 modulatory sites on NMDA receptors?

A

magnesium site and PCP

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7
Q

what must happen to remove Mg from NMDA receptor?

A

slight depolarization

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8
Q

what does the epsp look like for NMDA receptors?

A

slow onset and prolonged duration

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9
Q

non-NMDA receptors allow what ion in?

A

Na

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10
Q

what are the 2 kinds of non-NMDA receptors?

A

AMPA and Kainate

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11
Q

what is unique about AMPA receptor?

A

benzo site- inhibits response to NT

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12
Q

Kainate is the simplest receptor because?

A

no modification sites, activated by either EAA or Kainate

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13
Q

what does kainate allow in?

A

some Ca with Na

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14
Q

what do non-NMDA receptor epsp look like?

A

typical action potential

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15
Q

where are non-NMDA receptors normally found?

A

with NMDA receptors

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16
Q

where are metabotropic receptors found?

A

pre and post synaptic (pre= NT release feedback, not necessarily neg.)

17
Q

non-NMDA receptors are found?

A
primary afferents (direct sensory from periphery to CNS)
pre-motor (from cortex to alpha(upper) motor neurons)
18
Q

how are EAAs limited?

A

neurons and glia uptake system

19
Q

how do neurons and glial cells uptake EAAs?

A

Secondary Sodium activity

20
Q

what do glial cells do with glutamate?

A

turn it into glutamine and release it into ECF, neurons take this back up and convert back to glutamate

21
Q

Calcium that comes in the NMDA receptors bind to what?

A

calcineurin

22
Q

what does calcineurin activate?

A

NO synthase

23
Q

what is NO used for?

A

long-term potentiation and memory, CV/respiratory control

24
Q

what can NO do to neurons?

A

can be toxic d/t free radicals that can kill neurons and bacteria

25
If there's an ischemic event what can this cause? (mechanism of excitotoxicity)
O2 deprivation, cell depolarization, EAA release
26
what channel doesn't work that causes cells to depolarize?
Na/K channel
27
what else is activated by increase in Ca2?
phospholipase A2
28
what does PLA2 do?
damages membrane, acts on receptors, Ca2 from intracell. stores=> unfolded protein response, activation of eIF2alpha- kinase=> mito impaired fxn
29
activation of mu-calpain does what?
proteolysis and activation of spectrin and eIF4G
30
what does NOS cause in mito membranes?
disruption leading to activation of apoptotic pathways
31
what are the 2 things that activate apoptotic pathway to caspase 3?
cytochrome C + caspase 9
32
what is the danger of reperfusion of damaged neurons?
enzymes not normal, O2 becomes free radical
33
what does phosphorylation of eIF2alpha kinase lead to?
decrease in protein synthesis and activates caspase 3
34
how soon does the apoptotic cascade start after event?
4 mins