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Unformatted text preview: 1.)Ach comes from: acetyl CoA (generated by creb cycle) + choline (from diet)=AcH +CoA ** Rate limiting step= high affinity (therefore na+ dependent) choline uptake into nerve terminals Choline acetyltransferase (ChAT)= catalytic enzyme Juglone=ChAT inhibitor…(women w/ jugs, ur not gunna chat just stare) 2.) LIMITI NG FACTOR of rate limiting step of reaction= RATE OF CHOLINE HIGH AFFINITY UPTAKE **Triethylcholine (TEC)= inhibit high affinity uptake=most effecetive Ach synthesis inhibitor a.) High affinity uptake= sodium dependent, carrier mediated, altered by neuronal activity b.) Low affinity uptake= passive diffusion, provides non-neuronal cells w/ choline needed 3.) Factors that regulate AcH Synthesis and Storage: 1.) negative feedback= too much AcH, it binds to ChAT and inhibits catalytic ability 2.) law of mass action= Ach concentration proportional to availability of reactants and catalyst 4.) Same as vesicular storage as dopamine or serotonin except transporter is now Ach transporter “VaCht”- ------------VaCht inhibited by=vesimicol 5.) Termination of Ach activity: Ach released into cytoplasm hydrolyzed into choline and acetate by AChE( Ache has anionic subsite, attracts + charge of Ach and breaks ester bond). a.) Excess substrate inhibition= inhibited by high concentration of Ach 6.)Nerve gas= irreversible Ache inhibitior= too much Ach in body= fucks up CNS and PNS Drug treatment= a.) PAM=displaces Ache inhibitor, but doesn’t cross BBB so must be injected directly into the brain b.) Atropine= blocks muscarinic Ach receptors (therefore blocks receptors that bind to Ach, so less Ache binding occurs)...
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- Spring '11
- GABA, Muscarinic acetylcholine receptor, Metabotropic receptor, NMDA