week 4 tues notes
week 4 tues notes bio 390
U of L
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This 2 page Class Notes was uploaded by Mary-elizabeth Notetaker on Tuesday September 13, 2016. The Class Notes belongs to bio 390 at University of Louisville taught by Shira Rabin in Fall 2016. Since its upload, it has received 2 views. For similar materials see Intro to Immunology. in Biology at University of Louisville.
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Date Created: 09/13/16
Week 4, tues Tuesday, September 13, 2016 3:53 PM Diffusion of ions thru membrane ○ Movementof charged particle- conductance ○ Ion channels: Selective Bidirectional- diffusion in direction of electrochem gradient ○ Superfamilies- large classes that evolvedfrom commonancestor Studied w site directed mutagenesis- mutate part of gene encoding protein to change one or several AAs ○ Most channels gated- prevent mols from freely diffusing thru memb Only open in certain circumstances Regulated in 3 ways: □ Voltage gated- depend on charge on each side of memb K+ channel- two helices, cytoplasmic N & C termini ◊ Tetramer-pore ◊ Bacterial K+ channel- short AA domain selects K only P helix- selectivity filter pH change- swing open at cytoplasmicend--> conformationalshift(polar things move) ◊ Euk K channel- 4 helix voltage sensing domain Change membranepotential--> E force on S4--> mvmt of S4 relative to S5--> channel opens ◊ Open short time amt(milisec), close fast, stop ion mvmt automatically Inactivation, mediated by cyto domain(4, one for each subunit) Open pore-> want to plug it, plug removedlater to close channel New voltage chain needed to reopen ◊ Channel can be open/close/inactive ◊ Each cell has many diff channels controlling diff processes-respondto diff voltage/change Fascilitated diff- transporters help phyllic subs cross memb ◊ Passive, specific, regulated, saturable(at somepoint all transporters are busy) ◊ Solute binds on one side of memb->confo shift of transporter->soluteexposed to other side ◊ Ex) glucose transporter- causes confo shift, glucose phosphorylated when enters cytoplasm Normally few glucose transporters in memb, low uptake as transporters saturated Active transport- created/maintainsion/charge gradients(pumps) for K+, Na+, Ca+ and other ions ◊ Like facilitated diff…selective regulated and saturable ◊ Needs E bc goes against gradient ◊ Couples mvmtof subs against gradients to ATP hydrolysis ◊ Na+/K+ ATPase needs K+ outside, Na+ inside(3:2), pumps change Electrogenic- contributes to charge separation P type pump- phosphorylation causes confo change and ion affinity that allow transport against gradient Only in animals- evolvedearly to regulate Volume, needed for life ◊ Other ion transport systems Other p type pumps: H+ and Ca+ ATPases(ER)and H+/K+ ATPases(plants/stomach) V type(vacuoler)use ATP but no phosphorylation ◊ Light E used: bacteriorhodospinuses light E to transport protons out of cell – Some archeabac – First memb protein crystallized Light E activated retinal (euk photosnyth) Pumps proton out of cell Proton gradient used to make ATP(mitochondria) Cotransport- coupling active to existing ion gradient- gradients created by active ion pumping store E that can be coupled to other transport processes ◊ NA+/glucose cotransporter Keeps Na+ low in cells, comes back down gradient pulling glucose w it Can transport 20k-fold against gradient Glucose not phosphorylated- want to send out in blood Leaves cell thru facilitated diff Secondary transport- use E stored in ion gradient ◊ Plants use H+ not NA+ Coupled transport: – Symporters-move2 mols same way- one w gradient/one against Many disorders in genes encoding protein ion channels- affect channels on nerve/musclecells ◊ Exception: CF… 1/2500 kids, recessive(few heteros in class) Caused by defectiveCl channel- (CFTR)- pumps Cl- and HCO3- out of lungs, water flows by osmosis Bio 329 Page 1 Caused by defectiveCl channel- (CFTR)- pumps Cl- and HCO3- out of lungs, water flows by osmosis Ligand gated(cAMP)CL ion channel, bicarbonate transport, activationreduced import of other ions, causes thick lung mucus Over 1000 mutations □ Ligand gated- open when bound by ligand, not solute (neurotransmitters,cAMPon Ca+ channels) □ Mechano-gate-open in response to stretch/tension(haircells in ear) Membpotentials and nerve impulses- membrane potential generated whenever charged separated, in all cell types ○ Neurons- use changing memb pots to transmit E Dendrites- receive incoming info(short) □ Cell body: nus + met center Axon- long, outgoing info ○ Resting potential- memb potential of nerve/musclecell Measure w microelectrodes K+ gradients maintained by Na/K ATPase creating resting pot □ 3Na pumped out for every K in □ Outside more pos Action potential- cell stim, Na channels open, memb depolarization ○ Stim too weak- nothing Stim over threshold, voltage gated Na channels open->actionpot Quickly inactivated, K channel opens and goes down gradient, closed Some ions on wrong memb side, but charge change is only imp thing □ Pumpedback by Na/K ATP-ase Refractory period- cant do anything until charged up again na pump needs to go from inactive to closed "all or none" Local, depolarize certain part of memb, areas near it on right sense it and activate, and so on(cascade to right only due to refrac period) Signal propagates-> nerve impulse Higher intensity->higher threshold neurons □ Not depolarizationalong same neuron- all or nothing □ Can be restim faster after refrac period ○ Thicker neurons send signals faster- resistance to flow dec as diameter inc Limited approach, can jump btwn nodes to speed up 20x faster w myelin □ Myelin- sheaths neurons, lipid containing membsfrom schwann cells Na cant pass along it, Na pumps at Nodes of Ranvier btwn schwann cells Jumping synapse from end of nerve □ Neurotransmitters-premade chemicals storedin vesicles □ Steps: Signal in terminal knob Voltage gated Ca2+ channel opens Synaptic vesicle fuse w memb ◊ Neurotransmitterreleased, diffuse across memb Neurotrans binds receptor Ligand gated channel in target cell open and depolarize(excite)or hyperpolarize(inhibit) ◊ Depends whether channels are for Na or K Same neurotrans can have opp effect based on target ACh activatesskeletal, deactivates cardiac Norepinephrine stims cardiac and other muscles, contracts skin muscles Glutamate stim brain cells and GABA inhibits brain Transmitteraction terminated by reuptake or enzymatic breakdown(fastso signal brief on off) ◊ Many drugs block reuptake/degradationof inhibitors Bio 329 Page 2