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PSY396 MAY 22.docx

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University of Toronto St. George

PSY396 MAY 22, 2013 Lecture 3 Next Wednesday review as well Send questions by email 2 - Ap arrives at terminal button and change in polarization of membrane changes calcium channels calium rushes into cell and interact with proteins and vesciles fuse with membrane and spill vesicles into synaptic clept - Effect as long nts are around 3 - Reuptake – 4 - One way nts are removed form synaptic cleft - Reuptake by presunaptic neuron - But also by post and glial cells - Post – uptake nt from postsynaptic neuron 5 - Unidirectional comm from pre to post - But only predom - Post syn talk back in several ways - In order to reg nt and function of pre – reg feedback serves as message to pre to increase or decrease release - 3 ways post talk back to pre - Endocytosis – 6 - Pre syn receptors are protein that sit on membrane of pre and - Endocan – marijuana – active ingredient of - Pre syn button and post neuron and receptors sitting on pre membrane nts released by post and bind to pre receptors and produce some change in terminal button that affects neural transmission - Dendritc branch not all machinery for release of nt – so this is not calcium dependednt - Protein in membrane – membrane transporters that bind to receptor in post and through some change that with bring nt into cleft – intracellular then to extracellulr - One way post to pre - Diffusion - NO - Cell membrane – impermeable large particles - No membrane proteins involved - No in post and diffuses to pre in terminal - Endocytosis - Post syn neuron and released cell vesicles fuses with membrane releases to synaptic cleft and endocytosis is how cell injest things cthat cant make way through membrane – and the bt will bud in – pick up molecule and end up in cell as vesicle and end up in pre as nt in vesicles - One example all the way to dna and effect gene expression Autoreceptors - Receptors found pre neuron - Different involved in retro - One difference – auto bind to to nt released some liner in cleft will diffuse back to pre - In principal auto – different subtype of receptor of particular nts - These are exclusively meta no ion channels - And they decrease amount of nt released into cleft by neuron - Tell pre to ease up - Hetero – counteraauto – membrane pre bind nt not rreleased by nt - Sim on pre - Hetero bind chem. Released by something else – process retro or some other way - Autp released pre nt Nt - Class of preoteins allow transfer of chemical across membrane not act as ion channels Next - Intra – picks up nt and goes through change and end up opening extr side and allow nt to diffuse to extra space - And these are usually energy driven - Signaling from action comes from intra cell side - Three functions - 1 – involved in reuptake – membrane on cells around synapse and take up nt in cleft - 2- trans – basically fill – nt float in cleft and tran molecules pick up these nts - Multiprotein complex with enzyme that makes nt – usually bound with enzyme that produce nt - Transporters just take up nts - 3 – postsynaptic membrane transporters – and involved in retrograde transmission Mech of drug action - Def of drug - Compound produces some physc response and alter normal phys porcss - No good process of drug Some intro - Ligand - Mol or ion that binds to protein - Usually results in change in protein - Bidning site – active part of protein that actually binds ligand - Some multiple binding sites - Secondary binding sites mentioned later - Binding to occur complimentacy between chemical physical com of ligand and chem. Phys compositon of binding site - Lock and key model – fit between Lock and key - Ligand fit in binding site - Not just shape but also chemical strcuutre - Positive change area then likely have negative charge on ligand - Bidnign is very dynamic - Lock and key usually changes to both and chamges to protein - Lock reshape self to be more snuggly or produce some effect further downstream Ligan interaction - Free float lig and prot - And switch between l p complex and state they are free - Ligand something change in con while protein fixed concentration – not necc true making new proteins involve gene expression while most processes of lig and prot very short - Equilibrium that leans to l and p not being bound - Even in eq some of l p complex active producing some effect - When shifting away from eq add more ligand shift to right – more will bind and more complexes Saturation - Fraction that are occupied - Factors - Conc of l and p in solution - Also affinity between l and p - Measure how good fit between lock and key bwetter fit higher affinity - Even low con high affinity high prop bound Comp - Fixed protein and mult ligand can bind will be comp - Prescence of one or more ligand effect binding of a ligand - Addition of antagoinsit not produce reponese will decrease by taking up space Allosteric - Primary binding sites in addition most protein have secondary binding sites accesed other chemicals and these secondary binding sites are allosteric - Binding allosteric occurs ligand bind to protein change shape and open binding site elsewhere where another bind may change activity of lp complex All modulation - Active on extracell side another spot intracel that bind modulatry molecule - Allosteric can change binding site to make it more attaxtuve - Another is suppression of basic function of strcuutre - Change strucuture of primary binding site and change blocking phsy response Mech of drug action - Drugs can change main purpose of syn trans - Protein involved in nt likely drug that can affect it either synth or naturally occurring - Effect pre – syn storage release reuptake metab - Post – most proteins can be altered - Gene expression can effect strucuture and function Mech of drug action - Two - Ag and ant - Ag – compound that boosts phys outcome protein drug binds to - Can mimick but can other ways – can act like allosteric modualtors - Making the receptor more effective - Antagon – suppreison of response - Inhibit function of protein they bind to - Comp and non - Comp – one that binds to primary site and non bind to not primary site Next - Nt bind to receptor may be drug that can fit same way and produce physiological reposnse - However antag – chem. And phsyc allow to bind to active or binding site but not
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