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PSYB65 (Human Brain and Behaviour) - Lec 4 .docx

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Ted Petit

PSYB65: Lec 4 Short Forms: AP = action potential FXN = function PD = Parkinson’s Disease NT = neurotransmitter Neuron Fxn: -most info to neuron comes through dendrites -summed up in soma; if enough excitation, signal sent down axon -resting membrane potential = -70mV -ion channels (pores) in neuron membrane, whenever neuron stimulated, channels open up, allow Na+ into cell; when Na+ comes inside, inside becomes more positive; if enough input, enough Na+ will come into cell to make membrane potential reach threshold -when threshold reached, all channels in immediate vicinity open up, Na+ pours in, makes inside of cell extremely +ve = sharp spike = very brief and then comes back down ACTION POTENTIAL *whenever inside of cell becomes positive (not just because of Na+), it opens up pores in vicinity -positive-ness spreads very quickly so that more Na+ can come in -when AP reaches end of axon, come to contact point btn two cells = synapse (usu. axon of one cell contacting dendrite of next cell) -inside axon terminal = synaptic vesicles contain neurotransmitters/transmitter substances -when AP reaches end of axon terminal, causes synaptic vesicles to release neurotransmitters into synaptic cleft to bind receptors on dendrite (these receptors are connected to ion channels of dendrite)  allows ions (Na+) to move in  goes through same thing again -drugs usually involve some alteration in neurotransmitters Transmitters: -PD = underactivation of dopaminergic system; schizophrenia = opposite 1) Synthesis of neurotransmitters 2) Storage/protection of nt in synaptic vesicles (so not damaged) ; there are chemicals that disrupt process of becoming packaged; if not packaged, nt = destroyed = less nt available 3) Nt release; drugs can increase/decrease nt release 4) Nt interacts w/ post-synaptic receptor; chemicals can increase/decrease receptor activation 5) Inactivation of nt a) reuptake into pre-synaptic cell (recycle) b) degradation *generate drugs that can interfere w/ the various steps above; interrupting certain steps works for some nt while it doesn’t work for other nt Step Increase Activity of a Decrease Activity of a Notes System System Synthesis Increase Decrease Packaging No ways known to Ways to decrease -if not packaged, then increase packaging packaging; decrease nt nt susceptible 2 being from getting in vesicle destroyed by chemicals Release Increase Decrease Receptor Activation Increase activation w/ Decrease activation w/ mimicker (almost blocker (chemical that is identical to nt, can fit almost identical to nt so into binding site and it can sit on receptor activates receptor) but it’s not quite enough like nt to actually activate the receptor; nt can’t activate receptor because receptor blocked) NT Inactivation Decrease nt inactivation Increase nt inactivation (to stimulate the (get rid of nt to prevent neuron) continuous receptor activation) (I) MONOAMINES (BIOGENIC AMINES) a) Catecholamines 1) Dopamines (DA) 2) Norepinephrine (NE) Synthesis: DOPA  DA  NE b) Serotonin (5HT) Synthesis: 5OHT (5-hydroxy tryptophan)  5HT (5-hydroxy tryptamine) *DA, NE, 5HT are inactivated by reuptake (II) ACETYLCHOLINE (ACh) Synthesis: Choline + Acetyl CoA  ACh *Ach inactivated by breakdown by AChE *Ach found at NMJ (axon releases Ach on muscle) and brain -schizophrenia = overactive dopaminergic system = not MAKING too much DA; there are too MANY RECEPTORS = dopamine receptor blockers = drug = slows down system = if too slowed down, will be like PD patient -Parkinson’s = underactive dopaminergic system
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