Membrane Potential and Excitability PDF

Summary

This document discusses the concept of action potentials and membrane potential, including graded potentials, and their connection to ionic currents.

Full Transcript

yperpolarized greaterdifference btwninside outsiderestingmembranepotential drugscanalter polarization IEX notsend anervesignal restingusually 70mV 3Nat out 2kt in A fig find entia's createselectricalcurrent influx nat sodium requiresahormone neurotransmitter to openchannel Exam1 mostchallenging must...

yperpolarized greaterdifference btwninside outsiderestingmembranepotential drugscanalter polarization IEX notsend anervesignal restingusually 70mV 3Nat out 2kt in A fig find entia's createselectricalcurrent influx nat sodium requiresahormone neurotransmitter to openchannel Exam1 mostchallenging mustmemorizemicro principles positive negativeopposites iniloseproximity moreforce difbtwninside3OutsideOfCell Effigy threshold inordertoactivate fire astimulus maintain controlled response Nat dif btwn inside Natalwayswantsto go in alwaysgreatercharge t outsidethan inside outside Nat kt pumpoffsets theleak examquestions Ktgreatestinsidewantstotraveldown concgradient gooutsidecell greater Nat outside than kt extracellularfluid maintainsgreater charge intracellular islesspositiveisonegativepotential leakthrough concgradientthigh low Not truecharge justdifference btwn inside outside bothpositive butoutside is morepositive inrestingstate whenNatchannelsopenallows Nat in whenktchannelsopen allow kt out 3 Nat out 2kt out NO KI AKAmorepositive hopefullyreachthresholdfor activation bringingback to originaldepolarization state EX 70mV 90mV onechannelcan not depolarizeentirecell onlyregionalarea around channel becomes depolarizedlocalizedeffes Notlikeon offlights witch controlledactivationofconsecutivechannelsopening thresholdvalueinside ofcellmustachieve forgradedpotentialtotakeplace voltage whichligandgated changes chargelosesstrengththe greaterdistance it hasto travel doesNOTaffect entirecellis localizedto Channel hyperpolarizing viadrugcanprevent abnormalfiringfrom happening Ex anti epilepticdrugs Natinflux surface some kt lost chargeweakens signalweakensacrossthe musclefibersactivatedbyreleaseof neurotransmitters binding toligandgatedvoltagechannel Nat influx action potential travel to sarcoplasmic reticulum bodycanchangestrength ofstimulus3howoften it is released Gif frequencyofactivation howoftenneurotransmitter released Ex acetylcholine inskeletal musile Nat influx Not the ligandgatedchannel auseactionpotential blockrepolarizationbyblockingK channels muscleremaincontracted Nat Kt fat C1 contraction aralyticblockligandgatedchannel preventprocessfromstarting tofullystopmuscle weaken1butNotfullyblock contraction byblockingvoltagegated to Nat influx Nat kt onlyopenbychargeofsufficientstrength threshold tethered like aplug toopenclosegate Natdepolarizes cell mechanicalorchemicalclosingofgate Natgoextracellular 89 noplugmechanism beabletoreproducetexplaintheseduringexam 70mV Exineurotransmitt 141 19 NotinfluxIdownconcgradient 30mvimorepositidea.isue'Ensaenoutside hyperpolarization Itoomushktleftout mustfix RMPbegin dramaticspike in Nat decayedgradualflux in thattakeslonger toreturn tonormalthan Nat Na kpumpbringbackto 70mV Nat ktpumpstillworkingas normal Neverstops whether contrastingor relaxing Nat train iiit.i.in iin'i ii iiii Nat iin.imiiiiaiiis iiigiiiganonerone Icanbe inprocessofdepolarization thengetasignalformoredepolarization continued NOTjust one and down firing frequency Kt Kt tryingto rectifydepolarization now constantoppositionbutNatslightlymorepowerful itin activation iii juliaintopofeachother summation just b c yousendstimulus doesNOTmean cell will fire must be sufficient strength ofligandchanneltoreachthreshol triggervoltagegated actionpotentialneatinfl G howmuchneurotransmitterreleased highor lowfrequencyactivation into tell localanestheticpreventactionpotentialfromformingbypreventingNatfromgoing at painreceptorrespond tostimulus butblocksvoltagegatedchannels to stopactionpotentialfrom forming threshold activateAPforpainsignal to no Nat nonspecifichighaffinityforall channels bindtoneuralskeletal blocksalpha motorneurons asactionpotentialcomestoan end depolarization Prepolar ion car.gg 9tes fff sellcanstill respondto another signal untilMaxoutionchannel frequencyhowoftenneurotransmitter is released ease a Etetihote S 9975898areato ifeng.ies raopenup nextsetofchannels enzymebreak downneurotransmitterso channelsclose stop influx C Ithenthe channelsbehind itclose repolarize muscle connectivetissue Schwanncellscreatemyelinatedsheath to increase rate of propagationfiring Whereblocksconnect as Schwanncells slowconduction huscie neuromusculardefilit onlyneedion node channels withoutnodes wouldhave to wait for full depolarization to traveldown the axon lus justskifying largernervegreaterinsulation nodes faster velocityof action potential baseline 70mV APsw dif amplitudes amplification orturning downofsignals threshold in responseto Nat influx Dinchargebtwnpre postsynaptic canhavemultiplenervescontributing tooneresponsecombo ofexcitatory inhibito 8h's dsf h f Émf edmoren arrivefromperipheralns G'ftp threshold wrf9Yfapteelectrical activitycardiacsystempyrgginie y memorizeforexam gl g

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