Glutamate and GABA notes

For nmda r to function another synaptic input must

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For NMDA R to function, another synaptic input must excite the cell at the same time as the co-agonist (glycine or D-serine) binds to the receptor
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o Have a channel binding site that recognizes PCP, ketamine, and MK-801 (act as non- competitive agonists of the NMDA R) o Has 4 diff subunits o Antagonist = APV o Turning off NMDA receptors, stopping calcium influx 8 metabotropic receptors for glutamate: mGluR1-mGluR8 o G-protein coupled receptors o Either inhibit cAMP formation or stimulate the phosphoinositide second-messenger system o Some that are sensitive to the selective agonist L-AP4 function as presynaptic autoreceptors to inhibit glutamate release o Motor abnormalities shown in mice deficient in mGluR1 NMDA R’s play impt role in learning and memory o NMDA R antagonists impair acquisition of various learning tasks o Activation of this receptor necessary for induction of hippocampal LTP (process of synaptic strengthening – underlies certain types of learning) o Doogie mice, who have an overexpression of one of NMDA R subunits, exhibit enhanced LTP and improved performance on fear conditioning task, Morris water maze spatial learning task, and novel-object-recognition task Glutamatergic drugs of abuse: o PCP, ketamine: block NMDA Rs like Mg2+ Dissociative hallucinogens Non-competitive antagonists (like MK-801) Excessive exposure to glutamate and other excitatory amino acids can damage or kill nerve cells thru depolarization-induced- excitotoxicity o PCP, ketamine: block NMDA Rs like Mg2+ o Process mediated by NMDA R’s, some contribution of the other ionotropic Rs o One type of cell death = necrosis : cellular swelling lysis (cell bursts) o Delayed cell death = apoptosis : disruption of cell nucleus, breakdown of DNA o Excitotoxic cell death thought to be major contributor to brain damage that occurs in stroke
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o II. GABA 2 major inhibitory amino acid transmitters are GABA and glycine GABA synthesized from glutamate in a biochemical reaction catalyzed by the enzyme GAD (only found in GABAergic neurons) b/c of GABA’s widespread inhibitory effects on neuronal excitability, treatment with drugs that inhibit GABA synthesis (by blocking GAD) leads to seizures GABA taken into synaptic vesicles by vesicular transporter VGAT
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  • Spring '13
  • JeffereyLamoureux
  • Media, Glutamate, NMDA, NMDA then glutamate, block NMDA Rs

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