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NEURO 472 > NTs 4 > Flashcards

NTs 4 Flashcards

1
Q

synthesis of glutamate: where and from what by what. then what?

A

in neurons, glutaminase converts glutamine to glutamate then packaged and released from vesicles

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2
Q

glutamate uptake by? into?

A

into glial cells via transporters EAAT 1 and 2

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3
Q

after uptake of glutamate what happens

A

converted back into glutamine by glutamine synthetase, in glial cells

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4
Q

after glutamine is made, what happens

A

transported out of glia by SN1 (Na/H dependent pump) then back into neurons for resynthesis of glutamate

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5
Q

how to get glutamate into vesicles

A

Mg/ATP dependent VGluT1 transporter

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6
Q

glutamate transported into where and how

A

after action, glutamate transported into nerve terminals, post synaptic neurons or glial cells by an electrogenic process. EAAT 1 + 2 for glia, 3 and 4 for neurons

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7
Q

how do EAATs work

A

glutamate, 3 Na, 1 H go in. 1 K goes out. electrogenic

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8
Q

types of glutamate receptors

A

ionotropic: AMPA, kainate, NMDA. metabotropic receptors that indirectly regulate ion channels and 2nd messengers

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9
Q

AMPA channels: what ions? reversal potential? calcium?

A

influx of Na and efflus of K. reversal pot around 0 mV. there are Ca permeable and impermable AMPA channels.

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10
Q

non NMDA- R blockers? (2)

A

NBQX block AMPA. CNQX block AMPA and Kainaite

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11
Q

AMPA R general structure

A

tetramers: 4 subunits X 3 TM domains

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12
Q

AMPA receptors: subunits?

A

GLUR1 - 4, (aka GLUA1 - 4) made from GRIA1 - 4 genes.

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13
Q

AMPA-R subunit and Ca?

A

absence of GluR2 subunit = high Ca permeability and inward rectification

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14
Q

inward rectification meaning?

A

current passes more easily in than out. this is in GluR2 lacking AMPAR

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15
Q

AMPAR: rectification due to?

A

channel block by intracellular positively charged polyamines which are driven out of channel by inward current

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16
Q

Kainate receptors: structure? subuints?

A

tetramers of GluR 5 - 7 and KA 1 or 2 gene products, which have 3 TM domains

17
Q

NMDAR: block?

A

voltage dependent block by Mg2+, is blocked at normal resting potential (anything more negative than - 50 mV)

18
Q

how to mark glutamate neurons

A

VGluT (transporter) which brings glut into vesicles

19
Q

phasicity of glutamate action?

A

biphasic at + voltages because NMDA and AMPAR effect. monophasic at - voltages, only AMPAR are active

20
Q

D-AP5

A

blocks NMDA-R (competitive glutamate antagonist) so it blocks the second component of the biphasic action

21
Q

NMDAR structure

A

tetramers: NR1, NR2A - D. need heteromers: NR1 + one type of NR2 for a functional channel

22
Q

NMDAR permeable to? reversal potential?

A

Na, K and especially Ca. reversal potential around 0 mV

23
Q

NMDAR function? involved in?

A

increases intracellular Ca 2+. excitotoxicity, development of LTP

24
Q

NMDAR antagonists for

A

excitotoxic diseases like stroke and epilepsy

25
Q

how to activate NMDAR

A

binding of glycine or D-serine binding at the glycine B site (as well as glutamate)

26
Q

non competitive antagonists of NMDA-R (3)

A

ketamine: dissociate anesthetic. phencyclidine, ethanol

27
Q

5, 7 dichlorokynurenic acid

A

antagonist at glycine binding site of NMDAR

28
Q

metabotropic glutamate receptors: type and category and structure

A

mGluR1 - 8. monomers, 7 TM domains

29
Q

3 categories of mGluRs

A

1: mGluR1 + 5 couple to Gq and PLC. Group 2 = mGluR2, 3. Group 3 = mGluR4, 6, 7, 8. group 2 + 3 couple to Gi, open K+ and close Ca2+ channels

30
Q

glutamate excitatory but?

A

effects mediated via metabotropic receptors and sometime via second messengers can lead to membrane hyperpolarization by opening k+ channels or closing resting Na channels.

31
Q

mGluR and autoreceptors

A

inhibition of P/Q type presynpatic Ca channels by mGluR involved in presynp inhibition

NEURO 472 (15 decks)

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