Phys - EAA

Question 1

what is glutamate derived from

Answer 1

alpha-ketoglutarate

Question 2

function of NMDA receptors

Answer 2

critical in short and long term memory formation

Question 3

what needs to bind to NMDA receptors with EAA for Ca2+ to be let in

Answer 3

glycine

Question 4

what ion blocks NMDA receptors at resting membrane potential

Answer 4

Mg2+

Question 5

function of PCP

Answer 5

horse tranquilizer

- blocks NMDA receptor with Mg2+

Question 6

function of non-NMDA receptors

Answer 6

primary sensory afferents for upper motor neurons

Question 7

what is an AMPA receptor

Answer 7

a type of non-NMDA receptor that along with EAA binds exogenous agent AMPA or endogenous agents glutamate and aspartate that allows Na+ in

Question 8

function of benzodiazepines on AMPA receptors

Answer 8

bind to an extracellular face of the protein and decrease Na+ transport

Question 9

what is a Kainate receptor

Answer 9

a type of non-NMDA receptor that once EAA binds allows Na+ through and a little bit of Ca2+

Question 10

compare activation of NMDA receptors and non-NMDA receptors

Answer 10

non-NMDA: produces a typical EPSP with relatively short onset and duration
NMDA: produces long latency EPSP with a long duration

Question 11

how do non-NMDA and NMDA receptors work together to produce a long latency EPSP

Answer 11

EAA binds to both receptors once it is released –> both channels open, but only Na+ can go through non-NMDA channel because Mg2+ is blocking NMDA –> non-NMDA produces a EPSP –> this provides sufficient depolarization to cause Mg2+ to leave NMDA channel –> CA2+ can now go through NMDA channel and produce a long lasting EPSP

Question 12

function of metabotropic receptors for EAA if on pre-synaptic membrane and if on post-synaptic membrane

Answer 12

pre-synaptic: control NT release

post-synaptic: learning, memory, motor systems

Question 13

describe the limiting of EAA in the synapse

Answer 13

EAA in synapse is taken up by glial cell –> EAA is then converted to glutamine via glutamine synthase –> the pre-synaptic neuron then takes up glutamine and converts it back to glutamate and re-packages it to use as a source

Question 14

describe how Ca2+ entering the cell after EAA binds to an NMDA receptor causes activation of NO

Answer 14

calcium gets into cell –> activates calcineurin –> calcineurin activates nitric oxide synthase –> converts arginine into nitric oxide and cirtuline

Question 15

what are the four end results for NO after diffusing through membrane of post-synaptic cell

Answer 15

• diffuses back into the presynaptic ell and increases the release of NT
• works with long term potentiation of memory
• works in CV system
• released by macrophages

Question 16

negative effects of NO

Answer 16

has a very short half life and leads to production of free radicals, which in high concentrations are toxic to neurons

Question 17

what are the ionotropic receptors for EAA

Answer 17

NMDA and non-NMDA (AMPA and Kainate)

Question 18

describe the pathway for how a stroke leads to increased EAA in the synapse causing excitotoxicity

Answer 18

localized event (stroke) –> immediate loss of blood flow –> O2 levels near mitochondria drop to 0 –> ATP production stops –> Na/K ATPase activity stops –> depolarization of membrane –> release of NT into synapse –> uptake of EAA by glial cells is dysfunctional because it is Na+ dependent –> damage to neurons

Question 19

how does a stroke lead to apoptosis pathway

Answer 19

localized event (stroke) –> immediate loss of blood flow –> O2 levels near mitochondria drop to 0 –> ATP production stops –> Na/K ATPase activity stops –> depolarization of membrane –> Mg2+ leaves NMDA and Ca2+ enters –> activates phospholipase A2 –> releases arachidonic acid –> leads to more Ca2+ release –> activates eIF2a-kinase –> activation of calpain –> apoptopic cycle

Question 20

why does reperfusion after an ischemic injury actually hurt the patient?

Answer 20

kinases that have been activated take ATP –> ADP + PO4- and phosphorylate eIF2a kinase –> further decrease in protein synthesis –> further activation of caspase 3 –> further increase in apoptotic signaling