Excitatory amino acids Flashcards
Main excitatory NT in the brain
Glutamate
Glutamate synthesis pathway (most common)
Glutaminase catalyses glutamine to glutamate
The glutamate produced feeds back and inhibits glutamine (stops overproduction of glutamate) = negative feedback
Main method of removal of glutamate from cleft
Taken up into glial cells - converted into glutamine via glutamine synthase
Then released and taken up into the neurone again = recycling
Glutamate storage
High concentration in vesicles - have own glutamate transporter
Proton antiporter system
Uses high concentration of H+ ions in vesicle to pump glutamate in and H+ ions out
High H+ concentration maintained by energy dependent transporter
EAA metabotropic receptors: Group 1 - mGluR1 and mGluR5
Stimulate phospholipase C
Activates IP3 so DAG levels rise
Activated by trans-ACPD and quisqualate
EAA metabotropic receptors: Group 2 - mGluR2 and mGluR3
Inhibit adenylyl cyclase
Activated by trans-ACPD and quisqualate
EAA metabotropic receptors: Group 3 - mGluR4, mGlurR6-8
Inhibit adenylyl cyclase
Activated by L-AP4 and L-SOD
Act as autoreceptors
Resting potential difference in nerve cells
Around -70mV
NMDA
Agonists: glutamate, aspartate, AP5 Antagonists: AP5 Channel blockers: ketamine, magnesium, PCP Modulators: magnesium, polyamines Co-agonist: glycine
AMPA and Kainate
Agonists: glutamate, quisqualate
Antagonists: CNQX
Glycine
Enhances the response of NMDA receptors to glutamate (so bigger response when glutamate and glycine present in the cleft)
Magnesium blockage in NMDA receptor
NMDA blocked by magnesium when cell very negative
Repeated depolarisation leads to inside of cell becoming more positive so repels magnesium - allows passage of ions through NMDA
Ischaemia
Restriction in blood supply to tissues
