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Unformatted text preview: Biopsychology Exam 2 Review Lecture 8: Psychopharmacology PSYCHOPHARMACOLOGY: study of drug-induced changes in mood, sensation, thinking and behavior NEUROTRANSMITTER RELEASE: action potential is reached and causes a influx Ca2+, mediating neurotransmitters to be released from synaptic vesicle neurotransmitters influences postsynaptic membrane potential (causing the postsynaptic dendrite to take up the neurotransmitters)--Regulation of Neurotransmitter release: 1. DOPAMINE: VTA= location of dopamine cell bodies, which are projecting dopamine to the NUCLEUS ACCUMBENS (NAc); neurotransmitters are removed from the synapse rapidly by dopamine transports (DAT)causing dopamine to be retaken up by the pre- synaptic vesicle **dopamine on presynaptic terminal serves as an AUTORECEPTOR (feeds back on its own transmission and inhibits release of the transmitter) 2. MONOAMINE OXIDASE (MAO): enzyme that degrades neurotransmitters in the pre-synaptic cell (ex: MAO breaks down catecholamines) 3. AUTORECEPTOR ACTIVATION: receptors on pre-synaptic membrane that neurotransmitters can bind to, causing the membrane to hyperpolarize, causing the amount of transmitters being released to decrease (*dopamine autoreceptors=D2 family)**NEGITIVE FEEDBACK REGULATION! Binding of receptors: RECEPTOR (lock) is where the TRANSMITTER (key; LIGAND= molecule binding to the receptor) binds doesn't always fit perfectlywhen binding to post-synaptic receptors, the transmitter is activating/inhibiting the next cell Because neurotransmitters are produced in the body= ENDOGENOUS LIGANDS Drugs (ex: caffeine, nicotine, etc) from outside the body=EXOGENOUS LIGANDS IONOTROPIC RECEPTORS: control the opening of ion channels; FAST communication by directly opening ion channels; ligand-gated channel 1 METABOTROPHIC: ligands bind and INDIRECTLY open ion channels through activation of G-protein (coupled reaction); SLOWER REACTION but LONGER LASTING; involves ENERGY **neurotransmitter binds to G-protein coupled receptor G-protein activated causing G-protein ALPHA SUBUNIT to move to adjacent ion channel moving of the subunit causes the channel to open and ions flow across membrane FOR A LONGER PERIOD OF TIME (also the alpha subunit can bind to an enzyme (ex: adenylate cyclase) which PRODUCES A SECONDARY MESSANGER (ex: camp)) SECONDARY MESSENGER: activated by an extracellular signal (alpha from G-protein) binding to an enzyme (adenylate cyclase) which creates a messenger (w/ ATP) to activate an ion channel; these messengers amplify the effect of the ligand (the first messenger) GLUTAMATE: excitatory transmission; glutamate containing neurons project to striatum (region of GABAergic containing neurons glutamate cell projecting to a GABA cell which then moves on and dopamine is coming in, forming a convergence between the 3 neurotransmitters allowing for info to be processed in the brain); found in all regions of the brain; amino acid neurotransmitters...
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This note was uploaded on 02/18/2011 for the course PSYCH 230 taught by Professor Unkown during the Winter '08 term at University of Michigan.
- Winter '08