EEA and Excitotoxicity

Question 1

glutamate

Answer 1

made from alpha ketoglutarate

metabolic and NT pools strictly separated

Question 2

asparatate

Answer 2

made from OAA
doctumented as NT in visual cortex and pyramidal cells
often found w/glutamate

Question 3

NMDA R

Answer 3

ionotropic R 
post synaptic 
activated by EAA
allows Ca influx 
leads to EPSP

Question 4

NMDA R glycine binding site

Answer 4

glycine is a co-agonist, required for EAA to have effect but cannot open alone

Question 5

NMDA R Mg binding site

Answer 5

inside the channel
Mg blocks the channel
cell must depolarize to remove Mg

Question 6

NMDA R PCP binding site

Answer 6

internal to the Mg binding site

blocks the channel

Question 7

EPSP from NMDA R

Answer 7

slow onset - takes time to remove Mg

longer duration - Ca is slower

Question 8

Non NMDA R

Answer 8

ionotropic R
postsynaptic 
Na influx with some Ca
activation leads to EPSP
seen w/ NMDA R

Question 9

Non NMDA R AMPA

Answer 9

Na influx

blocked by benxodiazepine

Question 10

Non NMDA R Kainate

Answer 10

Na and some Ca influx

Question 11

Non NMDA R function

Answer 11

primary afferents, premotor

Question 12

NMDA R function

Answer 12

long term changes in synaptic strength
learning
memory

Question 13

metabotropic R function

Answer 13

learning
memory
motor systems

Question 14

neuorns and glia removal of EAA

Answer 14

Na dependent secondary active transport uptake

Question 15

glia cells removal of EAA

Answer 15

converted to glutamine and release into ECF neurons uptake and convert to glutamate

Question 16

EAA and NO NMDA R

Answer 16

influx of Ca binds to calcineurin to activate NO synthase to produce NO

Question 17

neural functions of NO cerebellum

Answer 17

long term potentiation and memory

Question 18

neural functions of NO brainstem

Answer 18

cardiovascular and respiratory control

Question 19

ischemic event mechanism

Answer 19

no oxygen so the cells cannot meet metabolic needs which leads to depolarization of the membrane
release of EAA activates NMDA R and Ca influx

Question 20

PL A2

Answer 20

release of AA from the membrane
physical membrane damage
release of Ca from intracellular stores

Question 21

Calcineurin

Answer 21

activates NO synthase producing more NO

Question 22

Mu- caplain

Answer 22

structural damage
elimination of protein synthesis
metabolic impairment

Question 23

apoptotic pathway

Answer 23

disruption of mito membrane activates capsase apoptotic pathways

Question 24

reperfusion injuries

Answer 24

oxygen is no longer used correctly

pi of eIF2 alpha kinase leads to decrease protein synthesis and activation of apoptosis