PSYC62H3 Lecture Notes - Lecture 2: Cerebral Cortex, Transporter 2, Nicotinic Acetylcholine Receptor
Document Summary
Open of voltage-gated na+ channel na+ influx depolarization. Open of voltage-gated k+ channel (delayed) k+ efflux hyperpolarization. Intervention and recreational (e. g. acetylcholinesterase [ache] inhibitor for dat) inhibiting the break down of ach. Synthesis can be anywhere in cell: soma (cell body) / terminal bouton. Transport of soma-derived nts microtubules + kinesin (anterograde) [walks vesicles to bouton] Docks at vesicle (t- & v-snare proteins; fuses w/ bilayer) Ap ca2+ influx protein kinase phosphorylates snare causing docking and fusion release. Snares can be targets of neurotoxins (e. g. botulinum [botox] premature cleaving of snare protein preventing normal fusion of vesicle) Nt cross synaptic cleft can bind either pre- or post-synaptically. Excitotoxicity: too much nt activity epilepsy (excess glutamate in postsynapse) & seizures. Removal of nts from the cleft often involve: Combination (e. g. glial uptake of dopamine & degradation by monoamine oxidase [mao]) Lock and key: complementary shape before nt binds to receptor.
