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Flashcards in Phys - EAA Deck (20)
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what is glutamate derived from



function of NMDA receptors

critical in short and long term memory formation


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



what ion blocks NMDA receptors at resting membrane potential



function of PCP

horse tranquilizer
- blocks NMDA receptor with Mg2+


function of non-NMDA receptors

primary sensory afferents for upper motor neurons


what is an AMPA receptor

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


function of benzodiazepines on AMPA receptors

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


what is a Kainate receptor

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


compare activation of NMDA receptors and non-NMDA receptors

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


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

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


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

pre-synaptic: control NT release
post-synaptic: learning, memory, motor systems


describe the limiting of EAA in the synapse

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


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

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


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

- 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


negative effects of NO

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


what are the ionotropic receptors for EAA

NMDA and non-NMDA (AMPA and Kainate)


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

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


how does a stroke lead to apoptosis pathway

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


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

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