Week 6 - PHCL 2600 Notes
Week 6 - PHCL 2600 Notes PHCL2600
Popular in Funct Anat and Pathophysiol I
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This 11 page Class Notes was uploaded by Emily Notetaker on Friday October 2, 2015. The Class Notes belongs to PHCL2600 at University of Toledo taught by Williams,F in Fall 2015. Since its upload, it has received 36 views. For similar materials see Funct Anat and Pathophysiol I in Pharmaceutical Sciences at University of Toledo.
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Date Created: 10/02/15
Lecture 18 Monday September 28 2015 1209 PM 0 Beginning of Repolarization Phase 0 Repolarization is the process of restoring the normal resting membrane potential after depolarization o Na channels inactivation gate closes o K channels are opening I Flow of positive ions towards outside of cell I Cell is becoming more negative Begins after eak iquot lzil39 z39 l ill l l39ii o Repolarization I Voltagegated K channels are open El More K ions leave the neuron El Buildup of negative charges inside of the membrane surface I Na channel inactivation gates open I Inactivated Na channels return to resting state Repolarization phase I produced by slowly opening of voltagegated K channels Decrease Na influx and increase K outflow causes the change in membrane potential from 30 mV to 70 mV I Eventually reaches below 70 mV and comes back OO o More negative membrane potential than at rest I Voltagegated K channels close slowly they remain open longer I Na channels are in the resting state 0 K channels close returning potential to resting levels o Resting Mb potential I MP 70 mV I K leaves the cell I Na goes into cell El 3 Na in for every 2 K out I Maintenance of Resting Mb potential 0 Depolarization I MP 30 mV I Na goes into the cell 0 Repolarization I MP 70 mV I K goes out of the cell 0 O Hemlralne oes not respond to further stimulation 0 Two tiies refractori ieriods I El During action potential stimulation H i l l li l 39 ill El Final end of active potential stimulation El Hyperpolarization O Stimulation can only occur after MP goes back to 70 mV o No amount of stimulation will produce a second AP PHCL 2600 Page 1 O Coincides with Na channels activation and inactivation 0 Channels will not respond I Inactivated Na channels must first return to the resting state o K channels are open and enough Na channels are in normal close position 0 Stimulation greater than threshold can produce a second AP I Need enough Na to counteract K efflux I Membrane is hyperpolarized to some degree 0 Possible to stimulate an AP I Must be a much greater stimulus I Still has to reach 55 mV threshold to activate Types of Propagation O nMimi r continuous conduction 39 quot ax s and muscle fibers a 7 r saltatory conduction I Myelinated axons I Propagation is more rapid I 100 ms I AP occur in between myelinated sheaths III At the Nodes of Ranvier El quotskippingquot affect Propagation of Action Potentials 0 AP propagation begins at the trigger zone near the axon hillock 0 AP regenerates over and over at adjacent areas from trigger zone I Trigger zoneaxon hillock to synaptic cleft o Propagated APT is not the same as initial AP 0 Propagation of Action Potentials o It propagates away from the initiation site One way I It cannot reverse direction El Previous axon segment is in the absolute refractory period Hi i i39lquotLile Ulsi if n 0 Step by step depo arization and repolarization 0 Flow of ions voltagegated Na channels in each segment ofthe membrane 0 Short distance propagation of the action potential 0 Each nodal area depolarizes to threshold triggering an AP I Ions cross the membrane only at the nodes 0 AP leaps from node to node 0 Ion flow is going around and through myelinated areas I Does not allow for sodium influx I There is no refraction in the myelinated areas Saltatory Conduction O Uneven distribution of voltagegated channels I Many Na and K channels at the Node of Ranvier I Few channels at region cover by myelin I Myelin increases the resistance to the flow of ions across the membrane 0 Buildup of sensitive channels at the nodes I Very small amount of channels in myelinated area Local Anesthetics Lidocaine o It is used topically to relieve itching burning and pain from skin inflammations o It is injected as a dental anesthetic or as a local anesthetic for minor surgery PHCL 2600 Page 2 o Prevents opening of voltagegated Na channels 0 Nerve impulses cannot pass the anesthetized region I No AP occurs I The patient cannot feel stimulus because it does not allow passage I Painful AP are being blocked Io Three major factors aect AP propagation o I Mielinated axons propagate AP more rapidly O I Propagation is faster in largerdiameter axons I Talking about micrometers 0 I Propagation at lower speeds when axons are cooled I Faster when warm 0 I Transmits information 0 I Receive information 0 I Where neurotransmitters are transmitted I AP is propagated further 0 Properties ofS na 0 5 I Action potential conducts directly between two cells I Gap Junctions I Cells fit together I AP direitly from one neuron to another 0 I Electrical signal is transferred from one neuron to another using chemical signaling I It needs neurotransmitters I Cells fit together I Abiliti to intercede with a chemical that could change the impulse or AP in some way 0 O Synapse is the junction between a neuron and a second cell eg neuron 0 Type 5 Axon and dendrite Axon and cell body Axon and axon PHCL 2600 Page 3 Lecture 19 Tuesday September 29 2015 1204 PM Transmission at a Chemical Synapse I rmlml loudhon quot where Jx ircaarwsnnissioh oi hemirrahsmiHeVs h pveSq nap HQ he AlOh OCQLAW s S l ePS Nerve UUkaAS 2 Cozd Openins MQMAX 5 NcmroHFOKHSMH l evs rdeoxsed Gee ll N t bind o anaconds 5 Li acnak Sosa channels open 2 mm in m to Posmhogp l ic waves 10A 7 NeVVCimxpudse SlMuoer 0 540 2 endoca os39 NT must be produced within a neuron gt i K W qu mg NTmstbeneleesedwhena Olka 47 Would NT I39D ComHWUKC cgt send Mpuusc a 39 lated d l 39 32 Lmtuw quot MusF be broken dovuh aFCW kzoSL Nanstbeinoctiveted quot F ILO39V after released 0 chief 1 argcr KcsPomses Released NTmust produce physiological responses N dlf a 2 Cause responses CS wlnltr xc39lrmfl39wWm 0 53 0 dircC l iowoeh w NT responses are modulated by Cahbloclc Visceralov 0V CW6 VeSporwse I I I I gt Made 0 gubcwq i iro e1 pamhdes u 39 Adn News on choliner ic synapse Lyecepi ovs Eioaenic dawnkeg care dCV39NcAHWS o4 owudvxc acids Puurines iii Ii39 l Synthesized and placed in vesicles Adcnos ihc melamine w vipoge 2 Pines group in axon terminals 39 39 Nwro Pep Hdes Synthesized and 9 xiYWHmegig packaged in a pVOle h gqnmiS OCLULVS We Sowm anal Hanna made have mus 030 0 eirmimls vesicles in sama Transported to terminals What Happens to the Neurotnansmitter Axon 0 Sending Neuron on mm 0 acivod ln on rece39winq mumow PHCL 2600 Page 1 Axon of Sending Neuron Elimination of o 39 newotransmitter from neurolransrmrerQ the synapse o 0 Activation of P0 IC m IH Te39ceotws Dendrite of Receiving Neuron Ohlq Na 0 OCH Node ln one Vece wincs neonom Lampendrric Pongy ap C 39 nunon Mum99M IntrocelldarWion m39 CplnephvincMr Neurotransmitter elimination ensures that the signal does not overstimulate the postsynaptic membrane 8 Spinal Presynaptic Cord Huron Nunm ltm 19 4 Nerve invoke a Postsmph iquot Effector Orgons Effect The response depends upon the neurotransmitter released the receptor and the associated channel Produce excitatory or inhibitory postsynaptic potential gt 4 he Poih lquot o9 gtltl From OKXoh Vminou emu me lo degrade hCWOtVQDSml HCVS gtcnd hcrc 51 Causes musclc Comm Hon mg he re 2 Causes air 966 Neurotransmitter released into the synaptic cleft binds to ligandgated receptors PHCL 2600 Page 2 avowequ Synapse Dendrite of Receiving Neuron W x l l wandgated inn Z39mnm39h Fast neurotransmission rapid effect acid Acetylcholine Glycine and serotonin XOLMp S 1 is a igand39 aw chanhe quot N l binds 0 receptors 2 ions Lido w An extracellular neurotransmitter binding site A membrane spanning domain that forms an ion channel 4 or 5 protein subunits Each subunit contributes to the pore formation in the ion channel 9 mekpocHqc pro veins hydro phobicquvopwmc ides Ionotropic Receptors em humus he In vow Cum mrxx w39rmb 10 Mutantquot chomugnc ncopton 6ABA is HM Bride Ciquot is ion Glow N06 ion AcePg Chol Wu Acetylcholine binds to the nicotinic receptor Rah bimer l3 quot MNPESD PHCL 2600 Page 3 B I I quot Pr SOGOdiorxs w G pro in SOMe vaeS 9 A end o be heA eroI Vimevric gt4 suglouew MS QGCC oh e FFCGOY pko t ih 399 CCD2O lo Q wamptr Chmnek 0 on channel 9 manager anaae goes hVLDLA5h OenO39l hCr C FFembr protein Slow MWMMiSSion 39 1th pnhm ourln nu plnn slow response No ion channel is part of the receptor structure Two different proteins They are to ionchannels Glutamate acetylcholine monoamines epinephrine and norepinephrine V dRP Fevew F on Chmnels W F mag be Cohh ed 9 0e Veccrerhm 39 indirect iowompic recaphoh PHCL 2600 Page 4 Lecture 20 Wednesday September 30 2015 1203 PM Metabotropic Receptors Slow neurotransmission slow response iltl fllh39ln uuplnl rn vplurx No ion channel is part of the receptor structure They are indirectly linked to ionchannels Glutamate acetylcholine monoamines epinephrine and norepinephrine Monomeric protein with seven transmembrane domains 6 protein couple receptors 39 Extracellular domain has the neurotransmitter binding site Intracellular domain binds to a 6 protein three subunits 00 7 064 AFC on mmx gt alp m be l oe quot Coe cd he iCroH lmerfc a 3 SMbmnlrl39s 3mm Metabotropic Receptors Mechanism of Action 6 protein directly opens 6 l indirectly open or closes an ion channel quoton n or closes an ion channel Direc Mechanism E7 Proflh39 PMVSc0ll 39 EMU 65 Memwsm C7 Pmcih rH39erOkCVS NI h2m e and produces ox Sascha messehf r O h s couud Cauge op hll O on Chanrwe rTTCVOxC l39S N ion CWOJWHCB 0 incl recArk PHCL 2600 Page 1 clmmopcacmm macaw WCWMOHKMWM 79xogwpg oz direc mecmwuswx S keps sends K ons OUc r o WW6 ca 2 Bud up 0 G5 Chw c oult dc C Second WESSer er pat5 0 C6 oss 0 hugBus 0V o4 her o New aha mowe complex 0 O Syrup A fiTPMFquot u is 393 u PHCL 2600 Page 2 ch as 1w MP PermeabilHx39 0 ions Grandes MP Receiving Neuron Ch es lw MP PermeabilHxl 0 ions GrandES 0 MP Weekes 0e scavenge iwvmbvrs 0x reayonse r u Ymn a quotwarm imam Wei97m Slight depolarization due to increased permeability to primarily Na and to a lesser extent Co39z EPSP increases the likelihood of producing and action potential I 39depensls on Postsown lt6 2 receplovs eps 39 ACh birds 7 Ope s Rom ohmne 3 Flow 09 Moiquot ions 9 dc poar392co membrane hcvcasc in m up um upwa 4nquotf lNhnodb um39 r I Tim nmwma39soc 39 q m r IPP slight hyperpolarization resulting from increased permeability to Cl39 or K Generation of an action potential is more difficult than usual 9 35 PB Steps C gtic39me birds 2 Opens ion channds 3 Flow 0 Clquot ions quotinto cc quot9 Mpekpokw izeo memeou e 4 damages in m ac i2 15 I n f E o A 2 7 3 is Wu E m 8 S g san i 3 W2 I 1101 39mi cl mien W t humming M Postsynaptic potentials are graded Small local changes in membrane potential Dendrites and cell body of neurons The magnitude depends on stimulus of channels Summation is the process by which graded potentials odd together Net result is a larger depolarizing or hyperpolarizing graded potential 10 39 Coezl H we pug Promx 0L over Gle o gouvcegb Depends on Whack maniacs 2 new many Chmnels are axe ve NOVKS For EPSY s a iPSPs PHCL 2600 Page 3 Summation at a Postsynaptic Neuron m WM mm 39 bu m k gt 1 FQ 9 i iquot 39 Kb u I m h B l ll W FlLACi WCSCA W 5 dimh l hemns omeare 1398195 2 EPSPS 9 Wig8636 Zone 0 he smmaf on Ce gpsxos 2 DSPS dccrmihcs th l hek RPS is Bahamaid rom incrc da kerm xnes Sum e GPec o QU Sfiwlqs Current Localized current Propagates Decremental it dies out Not decremental it doesn39t die out Threshold No Yes Distance Short distance Long distance Summation Yes No Amplitude Vary larger or smaller Same amplitude all or or size none Type Depolarization or Depolarization Hyperpolarization Place Sam and dendrites Length of axon PHCL 2600 Page 4
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