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Exam 2 Material

by: Emily Notetaker

Exam 2 Material PHCL2600

Emily Notetaker
GPA 4.0
Funct Anat and Pathophysiol I

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Exam 2 Preparation. Compilation of Notes.
Funct Anat and Pathophysiol I
Study Guide
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This 45 page Study Guide was uploaded by Emily Notetaker on Friday October 2, 2015. The Study Guide belongs to PHCL2600 at University of Toledo taught by Williams,F in Fall 2015. Since its upload, it has received 92 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 11 Monday September 14 2015 1154 AM I Cell pathology Since we are pharmacy students we would like to study diseases and the effect that drugs have on disease To do this we must rst understand pathology Cell dysfunction can happen If it is an isolated cell no real problem When groups of cells become dysfunctionalgt leads to disease gt problem is bow er a will lkO t39 need ieoLlel 4 PVObeV Rs wide 9 V aa issueDm0ye COMptcx y ms quot heedg 0 toe WeaL lQA g Cell reaction to m Cells are often subjected to abnormal to this in several ways alter in such a way that the cell remains functional but different a reversible damage is done to the cell because stress has gone past adaptation irreversible injury occurs if stress persists resulting in cell death Q Every Haian op csldc h body ism Fol39eh tial SW63 gt 4 1 i oes ouclrside harmed il ls a St39ress 9 Ex mmwrme Firms0 amounts of external stresses they can react 9 Wm S dwe l 49 oe sr39es 7 Home Stress is Presented Ou slole CeH COW k Zone operoda CHEF AdmHon Wm th 39 NCch Ex gt C 0 ab CSMDH Palm CCU but tlcetyw g Factors that determine process if a cell is mature it may adapt while an immature cell may die from the same stress better fed cells will be more likely PHCL 2600 Page 1 dew439 O F Q Okg enCIOr Vex cetl win kclvidt39e Cell has every PHan 4 heads Exi Vimin de P lCE CleS adapt while an iriirriai ke39c ii39 i y39di ri m the same stress better fed cells will be more likely Ex vi immin ole F idlencles to adapt rather than die in uenced by glucose and oxygen supplies if a cell had been injured prior may be more likely to be injured or die from similar stresses L2Crhccgnr 139 erqu prch Causes of stress for cells Lack of oggen remember this is needed for oxidative phosphorylation without it a lot less energy ThlS can happen by am M gauged w s kmlce or hum Hon Loss of blood supply blocked severed vmusdes 5946 9 u He on vessel neuroW 36quot Respiratory failur A h M Blood carries less oxygen CO poisoning hennan 9 O 3 L F C39eF E 39 395 E on how we anemia 3 being mkCh are OF qu CKWLlHS Mi GVQ g 39 CO Poisoning our XHQM3 Qdhcrnes s Causes of stress for cells u bacteria viruses fungi etc interfere with cell metabolism infections less glucose gt less ATP less vitamins gt less ATP coenzymes more fat ion imbalance lack of enzymes Down s or other proteins decrease in cell cycle mitosis Cwuszs ak ux 51 aLlc OF bmqh who sbk s Causes of stress for cells temperature trauma burns radiation Problem encountered here is often production of toxic substances such as H202 OH 02 which can carry one unpaired electron and are highly reactive these attack and degrade nucleic acids proteins phospholipids Take your vitamins A C and E I Swlaiocz admins hCC OCCAAJ S when wWVMWS Count lceeP LAP col SWQSSO S PHCL 2600 Page 2 s Causes of stress for cells an dosacja s A co hislr DRPS this includes drugs autoimmune diseases such as diabetes and multiple sclerosis body normally makes antibodies to seek out and destroy the foreign substances that get in to the body in some cases body will make antibodies to its own cells or proteins gt All V I oockl is arm Ping W SW6 OW her 0 H 9 Gorm an 01 l ew c remH on gt06 his e4513 C0t a e Weeded Adaptation does not mean that the cell does not change The cell changes to accommodate the stress and lies somewhere between a typical cell anda dead one AS Oh as H does e mgr agrsz pp ThiSis 0qi on xme 9 who irepear s What does a cell do to adapt Changes occur in growth and differentiation or shrinkage is quite common Egtlt Brain gt p as the cell shrinks in size because of a 39 over Jrime blood gecppk oei 0 brash lack of cell substances or cell number if 2 Cells beaux 4m QhVRDK in an organ or other structure due to to 0 Wm V9 330 0 lovedx decreased synthesis or increase in degradation of cell autophagy PHCL 2600 Page 3 Why does this happen Lochgem Decreased workload muscle Muscle isn39t worked as hard gets soft Decrease in blood ow brain Loss of cell number blood ow with age Loss of nerve input muscle Denervation leads to atrophy Loss of hormonal guidance ovaries Decrease in FSH andor LH Other reasons for small cells Stress is only one reason why cells can be small cells can fail to develop atrophy assumes that cells developed and then had to adapt organ fails to develo failure of cells to develop growth and development ends prior to full number of cells required for organ or other structure formation No WQOM draw amok mu s xze Park oi organ does ho k aevelcp 3 no l astral 94 size ovgm is ML l ROHOJ buds ho l mu Wig Y s What does a cell do to adapt MA ceu 1A u increase in cell size resulting in a corresponding increase in tissue or organ quot 59 M MUSCES due to increase in amount of synthesis of 9 Swen wz Ceug g a 6 structural components of the cell M do be we OC Mal Skeletal muscle increase workload on muscles W Ma they get bigger weightlifting Cardiac muscle increase workload on heart muscle due to hypertension heart has to work harder to pump against bigger pressures gets bigger Uterine size during pregnancy increase in hormonal stimulation estrogen gt smooth muscle NOJT amp S ooamp incmu in CCU i2 lh hw l 2 chlarew OP c aw is MUVWK Of htsFa F lQY S DHK how vch O rhtr amiss glso W n cell 39 i P WWWVVOPh is stvcwe or 00 long 0k 399lmil C mt is VMA CMlek Cells vol SQr 0 de eneVOL Le 9 bomber hear i PHCL 2600 Page 4 Lecture 12 Tuesday September 15 2015 1157 AM What does a cell do to adapt cell number and not necessarily increase in cell size still leads to enlargement of tissue or organ This can only happen in mitotic cells and that leaves out skeletal cardiac muscle and neurons this is an increase of total 7 1 63ka ugtll 51 Eh large Mice hleCFA WO OhV quotquot For att eienl reagon Mioic C us Ex eplAlheh39od ConnecA wc again the uterus during pregnancy may occur at the same time as hypertrophy if some cells are removed the remaining cells are capable of regenerating at least part of the structure liver will trigger hyperplasia in the other What iS it due to VWVWOPFW I if remove one kidney 9 4 aQOmWS gtltfak umio A hoch rs necessarxy 4 What does a cell do to adapt a replacement of one type of cell with another often seen in epithelial or mesenchymal derived cells An adaptive substitution by abnormal differentiation of a precursor stem cell Chw cs because 05 geresgor gt mislead in chronic awed ions PHCL 2600 Page 1 1m camera Real common in lungs of smokers Chronic smoker will have the epithelial lining of the lung replaced with different cell type columnar cells gt strati ed squamous epithelia These cells are more resistant to the smoke but don t secrete mucus smoker s cough and ma have a greater chance of infection This is a reversible reaction its not automatic th t cancer will develop 1 However this is one of the precancerous conditions that does transform into lung cancer gt Harder 0 Li w i incewa Ocu m is prbolLkc l wc laqu 9W up SHH an adap ve sl moe How I a Not an adaptive process common in epithelia Related to metaplasia and hyperplasia See variations in size shape and developmental organization of cell in tissue see a lot of immature cells Changes are seen in nuclei shape size Premalignant condition cancer Seen in epithelium of respiratory tract Seen in cervix Implicated in both cases as a stage of cancer development vf EmmiW knch cells cu in he Sarina Placc vol dl GFeiCh l szaes lnoqa 7 W 04 dcvcloioihg 0k 99 lasick Occurs when stress reaches limits of what cell can do to adapt Membrane damage Swelling of mitochondria Swelling of ER Golgi ribosomes Chromatin clumping 9 3th DNA is no lo er Addac hwok l o rccmm caused wxl pH Chmegt Al gushg Cad 0 Ce deadla iF coanued PHCL 2600 Page 2 Membrane damage Chemical agents and physical agents may make holes in the membrane Cell swelling due to increased intake and no control of intake of water Na Caetc Leakage of enzymes is possible Leakage of K is possible Leakage of protein is a diagnostic test SGOTserum glutamic oxaloacetic transaminase WHCI W virlneSC ehzq mes so FVCVEQSQ S O si w LDH lactic acid dehydrogenase E I CKCrea ne kinase Hood ceHS cure undergoing mac deo A 39 Leon W ine exwzqmes in latoool css Happens OF er When 2 dVLKSS owe used Ainqairini ng inside he cell can canoe owei 3 Q s Swelling of mitochondria Due to ion imbalance and resulting water uptake Due to failure of active transport systems NaK ATPase W vgtCUihg 0 WM cmponervts goes Prom k OUC VCV 0 inner g Swelling of ER Golgi ribosomes Formation of blebs or cell surface pieces of membrane Due to swelling controlled by an increase in anaerobic metabolism and the corresponding decrease in ATP Ribosomes detach from the ER T No Pr duc bh OF Pmk ns NON ook ins 63 how ohs cell has o souviVe LlYVeveirlblc W WEEroveV GD s Chromatin clumping Chromatin condenses and clumps 3 PH 5 getting Won ovuef dcnamrod ion Without mitotic actiwty Due to change in pH lower than threshold necessary for proteins and pVorcihs beamu 0 akenodwe PHCL 2600 Page 3 VVILIIUUL IIIILULIL OLLIVIL Due to change in pH lower than threshold necessary for proteins and nucleic acids in chromatin PVOTClh lo M o dangtum whoF CVemre more prorein lpc PoyW VS O 41 PVOCC are i r13 unread quot C6 is Oi tode Ce dm HN gt irreveysilole WV COxerable iAll injury Can be reversible if only transient Can become irreversible if persistent 10R more than a few hours This results in cell death 9 9 2 Sl39eios vest ch aura Wheh W8 Qnor l perRed o9 ime quot cell hag ChCK ed loud is SUQVivll 0 NOW ILJJheiodoh 0 more lhbpxr h h Fwdcure k Lasa Z gaps quot me ion CCU aim shovk is depend enl on iCell death Two patterns more common occurs usually as result of external stressor less common more controlled is programmed happens even to healthy cell populations during development Less ATP lo 39lr g rvxccle3 cell Pang Hon is no l as good o die For VowOMS VQQQODS Lor m gets 00 large immmotoiaicod Veagohg Squot Due to ischemia loss of blood supply 02 or chemical injury Severe cell swelling and possible rupture of cell membrane folowed by in ammation Breakdown of organelles Protein coagulation cytoplasmic proteins will irreversibly form clumps of protein Usually happens after a few hours of exposure to the stressor Max 3MS gt dependka or C l wpe L baaGem meres C dead w Ni OCCLKV PHCL 2600 Page 4 g Nuclear changes with necrosis 39 nucleus shrinks until it is nothing more than a blob of tightly packed chromatin chromatin disappears due to digestion by Dnases from ruptured lysosomes 39 nucleus breaks into clumps and is extruded through the cell membrane 9 size 09 humBolus Lee beeps 3 Sl 039cj quot some l hihfs gt SitAHOQ 0 Wuhol lh Wm il meKS lokobS 03 361 3 via 0 Regulated event Can occur in normal cells during embryo development Regulates number of cells in tissues Can eliminate potentially dangerous cancer cells occuws dunlij developmenl 63 F Grams L NhCh CEUS so laced 9 CMC Y roo in oqu cc Hxod cavxvxo39l be got rm rid o F Pasl enough Apoptosis continued Chief features are Chromatin is condensed and fragmented into small dense masses Masses gather near nuclear membrane and are extruded n Apoptotic bodies residue of organelles chie y form and are extruded PHCL 2600 Page 5 s Abnormal cell growth Two types controlled or reversible usually occurs because of a stimulus stops when stimulus is removed Hyperplasia metaplasia dysplasia irreversible uncontrolled persists even after stimulus is gone competes with normal cells for nutrients steadily Increases numbers regardless 9 Comeres we vetHm miner GEMS inceaan Le gize lel Characteristics of neoplasms Benign Malignant Closely resembles Anaplasia often normal tissues does not resemble Slow progressive Could be slow or growth W39quot Stop fast invades tissue usually encapsulated and is localized 39 Non39encaPSUat6d Does not and invasive metastasize Frequently does Encamuloctedt m OklOLMkd H Ae osoizc breaclcg 0 ehevs CRlCUKOcHOh Md moves 1 a new wage acdge s CWC Ix lavomen dotOW V 40 Wow vvxodH xl PHCL 2600 Page 6 Lecture 13 Wednesday September 16 2015 1201 PM Liver cell Swollen ER 39 a de s ma jquot ER nbosomes 39 swouem 5 mitochondria quot ei is 39 Tuberculous lung Lymphoma Cells undergoing PHCL 2600 Page 1 at quot A 39V ff 5 Vso son10d C h VW3 Ml COLdd be dues 40 bacAcrlal inPecHovx Lymphoma Cells undergoing 1 JC Crss section of heart Left ventricle 0f the Brain iMf qx 39ZC r I v 39 PHCL 2600 Page 2 Sweng5 Phne VtVLg GKCeP 2 Pmmouunced ARMrows a d39eCDMPOSVHW Pancreatic ducts 39 Adenocarcinoma of colon DOCS Mx Aedomg ofthyroid IODks k6 oolc we om mm US gems PHCL 2600 Page 3 Lecture 14 Monday September 21 2015 1153 AM Neurophysiology l Today39s Topics 0 Nervous System 1 Overview e Reading Assignment 4 Principles of Anatomy and Physiology 1439 Edition 6 Tortoro and B Derrickson n Nervous system Chapter 12447484 Divisions of The Nervous System CN CCWWOLJ 0N9 vet Pherod Sensory and motor fibers CNS to muscles glands amp sensory Center of the nervous system Connects the nelves receptors brain and PNS 39 uripheml 5 quot 39 9 Clister of neurons nervous system Nerve fibers House inside vertebrates CNS Functions Control of voluntary movements Vouhmrl g J39h Contraction of muscles An A PHCL 2600 Page 1 has loue Mada gow book do IhVDl WW4 boom nativeCAN coorics oeki Vouhmr h39mas Ioue Mouse gow may do InVDl WW4 book mad udmdw carrKCS OLA l Process 3 not hou3 vd ampW Control of voluntary movements Contraction of muscles Control of involuntary movements Breathe D39geS on of fond MZSSCKQQC COWS ln l nVOU A OxFF rehl39 WV 2 Wrad wa ccmcr CNS Processes 3 Sends OLJK V messacsc AdmWk chcn nerve Processing of incoming sensory information E Source of thoughts emotions and memories Gal64w Peripheral Nervous System Divisions 395AMPNS a Clsbd V9 3M respohgeg OFVaLUtquot Jvoece on CJnadl evwae w WWW 7 PM gVquotquot rueh MM chant e moCNS kg 0 p second dcosiow I V Nor cornSciouxslxi accideol w 3 Ex Foucle OK bear PmraMS mgnl umquotmm Re ix 236 33193 25 nucum nonmam 3 MOs V aback ed W earl4V3 rm names EX 60 ng sleepirw Organization of the Nervous System Wmammmmmg Incoch mm OLLA VOYWOKNUCS 7 aiLhMONC gt 60mg o bOCHMOOVVL s Earned C sumac gt 9 learned Vespoh zs mrmmemmumw Cell Types of Nervous Tissue Mogq be able to remir gnawkw 39 Transmit information from one cell to another They do not divide Neuroglia or Glia Cells Provide support nourishment and protection for the neurons They divide They outnumber neurons ueppoiA39 Lek S I WWquot 394 PHCL 2600 Page 2 Parts of a Neuron Delulvilnt 7 J Nucleus Neuronal processes Extend from the soma Long and single projection Propagates nerve impulses Cell Body or Soma Metabolism and synthesis of proteins for dendrites axons and synaptic terminals 39 Receptive area for synaptic inputs Specialized organelles nucleus RER Golgi mitochondria lysosomes Nissl bodies are group ribosomes 191wa K Cellular movement from Shape and support Im Tree like structures extending from soma Expansions of cytoplasm contains some organelle Receive signals coming from other neurons cm 9cm r Major site for synapses Presence of receptors in postsynaptic membrane in F r s l 1 when It propagates nerve impulses away from soma It contains mitochondria amp cytoskeletal elements It can be wrapped with myelin use PHCL 2600 Page 3 1w KW CO DzV dhA es QMVZ cell myses Rxovx whcvc can Sands OLJC l vd o SN RPl ic Aerm u od S 39 Plouces w here mwon race Wes impact Nl bodics grouped ribosomes innle 0 lame fS impuxlsa prowe oele a er IAAJ It can be wrapped with myelin Myelln helps lmpuxlga propaSoele agtev Axcn man We m calmer Axon cytoplasineimw 1 AIM Creedeg as m elin Sheosl Plasma membrane Axon Structures Axon joins the cell body Part closest to hillock Junction where nerve impulses arise are side branches Back to soma or other cells A quot 0400 Wmlha S Terminals Form synapse with another 39quot quot neuron Mauro Wsmi l lcir 9 glared released in hc sqrwmp rlc KnOb 0 pro Gagatee impudse Very S yiaptic Knob lme taxPensions 0 moms l Site of communication Neuron to neuron or neuron effector cell Synapse consists of H l lmPorkochi Wl lnc ceH has reccgalors TOW hc hCm39lrrmSmlHtr lo bird Contains synaptic vesicles wit neurotransmitters 9 Presxp ocpHc ending quot latter h0P v in ne axon Poe Xgs noquc mendaroch ova er sqnocPsa m h dendrite snnoeprm AC Pk OOS OP h wvotraanMilto s VC a ecl hem l WaySW 0 6 plwpower accwagq Contains receptor sites for neurotransmitters Gap between presynaptic and postsynaptic cells 0 Types of Axonal Transport I cellular process responsble for mvementofcellcomponentstoudfmmthesm From soma to axon From axon terminal terminal soma uses microlubulcs tam termncu PJCIOUOUCS Axonal YrOnsood Axonal Transport Uses Microlubues PHCL 2600 Page 4 Transport to axon h Slow axonal transport 39 Moves neurofilaments microtubules 0110 mm per day Fast axonal transport Moves organelles with membranes eg synaptic vesicles mitochondria along surface of microtubules 50500 mm per day Mediated by EL 7le 17 712 4quot quot goes FVOM W 9 axon 1quot I Aw rue r 2 Transport from axon quot t r39 terminal to soma Jay W Fast axonal transport a V Moves membrane vesicles and cellular material to be degraded or recycled 03063 WOM axon 0 soma Moves substances that enter the neuron eg nerve growth factor tetanus toxin and viruses Mediated by Evenm Arrangech mar r39o W meC i ex vecdclin 5 Mandi F39lcac OMS 39 Head binds ATP and More complex than kin microtubules Multisubunit protei Tail binds cargo Accessory proteins It moves along Kihcsin Qoocs N46 H5 microtubules tubulin 0 3mmquot of has lb m39wah39 Along 1mm Inrl hm t 39 m m AD Aquot c I Iona n t 2 I M Ownein quot mcceSO pmihs O Minedum 0 danCl lh 39 needs o rlner Wing Jro Wc Hovx composed OP WW ll Cl cmxns w 1w nhH u httple uic aMclasuxbo39osbioleOncmn39kimm hm 0 Haber Commam ko mzessm FWDtellng o Q r heavy Names 040 mmim PHCL 2600 Page 5 Lecture 15 Tuesday September 22 2015 1159 AM TopHat Code 209703 Types of Neurons Neurons are classified based on structure on function Accordi to the number of esses extendi from the bod quot9 Car 2 Pm pi quot9 Y Multipolaru bipo or and unipo ar neurons Based on the direction of the nerve impulse with respect to the CNS w One long axon Multiple short dendrites Neurons 39 Motor neurons Neurons in the brain Neurons in the spinal cord Coll Denomos oooy Tnggolzona T4piCO WP 0 th Myem sham I Axon erw tomnu J quot v 39 K I 5 l x a Mumpoiar neuron Two main processes One axon One main dendrite Axon and dendrite are on opposite sides of some Location TW 0 Often sensory neurons Retinal neurom eyes Auditory neurons ear Olfactory neurons nose d F r h pokes loi polars PHCL 2600 Page 1 39 Cell body lies to one side W One process divided in two 0mm T I W branches quot 939 like 0 proHMSlon Anon Axon and dendrites are continuous and extend in opposite directions Sensory neurons in PNS 39 Skin 39 Muscles 6i joints Internal organs cthookrneuror Can oooy wean sheath 4 Sensor A Gereh 4 where iiLFo comes iw gt npukl MOl39Dl E F cr r v where info 3065 cud OLJCVPLL39l 39 Ihicrhcwons gt Moxie associach on blob hc Sangerx ihpucl 2 modor ovum WCWOHS Neurons Functional Classification Sensory impulses from receptors Sensory or or sense orggns to the brain CNS A QFw39crchr r Sensex Memos m Most are unipolar neurons 7 39 a A A Comect sensory newon and h In motor newons Locmd mainly in the ms In lcrhcmns Multipolar neurons V 39139 Motor or efferqn 7 Nanon quot l j if j Carryinfo fromCNStoperiphery E Effectors are uncles and glands Multipolar neurons E FFCVW Motor NW inl c voetcs Moior ouck viers Wod broqn is ying to cudpud 0 Paviphcry l39r lt wr 39 Q w W I In the cerebellum Motor function Pyramidshaped soma In the cerebral cortex 1 and hi pocarn 5 m m J AA P MPjiAL 5amp4 ma PHCL 2600 Page 2 Pyramidshaped soma In the cerebral cortex 1 and hippocampus it x 77gt Memory attention w language and thoughts Au D e in hose vol developmenl oq RSgues 5 quot39 Hard 0 ocucs QnOVl cal lam Hon 3mm Limcraaocr gealole Neuroglia do not generate or conduct nerve impulses They can divide tumors gliomas 39 WV cure con Sacred canes They support neurons by rms much 9W trade 0 Forming the Blood Brain Barrier BBB Forming the myelin sheath nerve insulation around neuronal axons Making the CSF that circulates around the brain and spinal cord Participating in phagocytosis 439 Clean up area Mira hem Types Of 39 Sou keua gt go 0 Two ccquot fypcs in 0 Four ccquot wpcs in Id 9 WM Q Ma 0hv00m Gorwx wrap gelwok m cell COQCOVK am quot Asl ro Art63 chuse o P heir praQacHorws t 39Sod39cl il C 9 NOYK 4 036Hwev on mp 0 max 0 veron eelOW mole book 39Schwcxhn quot wraps m axon levels sand was I 93mm Surouxl axons PNS o No responsibly lav myelnahnn 01 poiWm axons O PaniCipate in W process amquot away PHCL 2600 Page 3 LTC 39IM39CCS law an Cm CMU wmqovng Jv camw ma Lmom bbran we I Fun on zlmctmt Dvmm 511mm mm amu Requisit m fumequot and mowed c CU K39UWJI A1 5 39 OI isodehclmcfes Q39vallour 2 schmanCBRS MlCJO HR 9 060xVM e mm h UUOhs 0 WFOQW Semi permeable barrier Composed of blood vessels and glial cells astrocytes Astrocytes processes cover capillaries 9 wFoo IJ process M6 W Jr agree Capillow39xe39s quotquot CClC it W 1th h0cl prom 9 Hak l dudc orws preVei so ucke Malawivi WitQ hdohellcu calls Keeps macscrlau WM Ccs BloodBrain Barrier Solid connection between the adjoining vessel wall cells Protein complexes known as tight jmctions Prevent diffusion of material between endothelial cells Special transport systems Myelination Myelination is the process of forming a myelin sheath which insulates and increases nerve impulse speed Myelin sheath 80 lipids 207 proteins and water It is formed by Oligodendrocytes in the CNS and by Schwann cells in the PNS Multiple Sclerosis result a y gyms Wyn u r39vwlmalod dun from autoimmme destruction of myelin PHCL 2600 Page 4 gt kdePihj mosV16 CNS 39 13l er haclquot onlq ampOWS car mum Awhin g vaou h CgeMipemnWecuole a g 4 0 4 0VN VC cond ULCA39KW 5 Axons no o W OKV surrounded b mqelin gt when bun a 0 4 wuouuse Speed 13 I034 u 39w 1310 wuw Ll Numbwed u Multiple Sclerosis result fgom autoimmune destruction of myelin Y e 139 a Lexorxs no 0 er are suurrouxnded bl mqe n when amq 2 4 MpLJkS speed s log PHCL 2600 Page 5 movemer s Durexch Souo or do who mom 04 ow Poor per gtmmce kudox39mmwe mcasOS ne mexc SSquot Cm VCCOthi CG somCAhlng n louur mdq as bang somewer bra 33h hod needs co be degVoqu 9 immm s erem is QLKPpOWC quot D 4 rid OC hr s ha mi make wove 9cm Lecture 16 Wednesday September 232015 1153 AM M Each Schwann cell produces part of the myelin sheath surrounding an axon Wm A cell myelinates one segment of an axon Cells wrap around PNS axons Inner portion is d rher em s HH Pow Hons 44006 are nod mxiellm hsd 399 cm ed Modes 0 Radxvle Outer portion is the u waamamxn tmdsmlt nar AutumnVIII IOti Mm Ibom manqszmulu Mann so 1quot khnm onno uvwwmo quoton mega u 1m NA 3 Cu mu 1 A Inland non if none Dul n w hunt111510 HUI II Iquot flourQ sHC l Chlh 7 lon drmsl wwaaegb Each oligondendrocyte cell forms myelin sheath around as many as 40 axons in the CNS Cell bodies are small Have nodes as well PHCL 2600 Page 1 Cell bodies of oligodendrocytes do not surround the axons 39 No neurolemma is formed 39 Tip of processes is involved in forming the myelin sheath Synthesis of large amount of plasma membrane Krone LAP 39 7 Cfea heah n 39 Mammmmmnmqmm 3I No swimC Olel quot No an 39m SkaHom 39 Unmyelinated axons are a bundle of axons that are wrapped very thinly by 5cm cells ID a cuseir Facilitates the rapid conduction of nerve impulses 9 VeVH qugd Electrical impulses hop from one node to another 0 Now 1 WW6 Med 3 SONr 0 Periodic gaps in the myelin sheath jgt 44on Mpqueg com uck down an oagtltoh neutron PHCL 2600 Page 2 H Presynophc m Activation of presynaptlc neuron 39 Action potential Communication at the synapse Release of neurotransmitters Activation of postsynaptic nailon Activation of Receptors Transmission lit 9 Pow neuron Neurotransmission Production of action potential Change in membrane potential Flow of ions 39 Release of neurotransmitters at the synapse We in Neurons Like muscle fibers neurons are electrically excitable They communicate with one another using two types of electrical signals Shortdistance communication Communication over I distances wi in the body Electrical Signals in Neurons Production of electrical signals in neurons depends on A variety of ion channels that open or close in response to specific stimuli Because the lipid bilayer of the plasma membrane is a good insulator ions must flow through these channels Exocx osis gt A tault36 1 0 neuvomgmi k tevs go Whipuse is rcccv dl l CVlCOJRI calwen chem COKH drive ace Hon Po l en l ioA Caugeg some rhm The existence of 0 H PHCL 2600 Page 3 Jn ha mph folAMPC QMP quotWWWquot I u guvu INSUIUIUT IONS quotIUSF IIIquot through these channels The existence of QC HOVN POAen HoA Caugeg W W h O MW CCJANSCS QM P Type of Ion Channel They are present in the plasma membrane They randome open and close They open and close in response to a stimulus 39 3 pf39m m39iquot f quot7 Ligand chemical binds 39 39 Specific ions cross the MCChOJW lCaJ 9OVC O P s 39 mmb39m quot d mmquot f gt Velmaa ea Fri M 0 Opams concentration gradient higher to lower 9amp0 Sl hod needs 0 be bow o he Shamel 39g 2 liqWinn WowquotMound W Iiimanna EWWW Imam Permeability to ion is high They alternate between open and close position quot Vahdom 39 Present in all cells In neurons they are in dendrites cell bodies and axons W I 5W m Mm mow Cytosol u u I Binding of a ligand stimulates the channel neurotransmitter hormones and ions 39 Iquot damn f sensory quoteuroquot f TellS W NevaOMS Nhod l o do In dendrites and cell bodies of interneurons and V motor neurons mainly concentrated at the Oh PCS rng P HC Ce synapse atheroc res mpudsc PHCL 2600 Page 4 W I Eurcolu M Ploun mamn Cytood 39 vibration touch pressure and tissue stretching In auditory receptors receptors in internal 9 i organs and skin receptors slam W5 0lON LAS l o F burh sewageH ons W EIB MWM gammamow CY M Open in respond to a change in membrane potential p mainly located along the neuronal axon v depolcun Zodl39cm pokoquM i im Generation and conduction of action potential in axons Present on unmyelinated axons Node of Ranvier myelinated axons and axon hillock Na K and Caz channels Model for VoltageGated Na Channels Example Na channel Both activation and inactivation gates need to 5 be open for ion to pass through At rest the activation gate is closed and the inactivation gate is open Voltagegated K channels has a only single gate PHCL 2600 Page 5 Lecture 17 Monday September 28 2015 1154 AM i I Iiilm R 39 we 5 MP ls med d at r Extracelulerlluld PIasma membrane Cv osol neuron is not conducting a nerve impulse L Buildup of equal numbers 4 V of negative and positive ions in opposite side of n in lwllnzlimimlm L l 1 r l n U V up i 1quot mm aquot Him umhiu39uimmil i v 9539 95 71347135 Buildup of charge occurs only very close to the 39 1 membrane 39 39 a Distribution ol charges that pvoduoe the resting CYfoso sewme in n membrane potential olaneuron cell is electrically neutral quot39 r e 1 I n Resting Membrane Potential Ibifferentlmconcentra onsacmstheplaunam d Winnem depends mlntyonx39andNa39 Ned05 eat 06mm LAN Ml us Mfg Fahd e InsidettlenetmK39lslighchugeisbelncebynegothely chagedluumdprotelm C a 2 are M C0 powkoavl t39oo WMMNaWs Na isbalance Ci39 w quotW De pends on Mod a C mos Ha 0 Na is begocnced m Cl C by A y 3 1320713 N Membrane Potential i lu iimr ui L lynx A L m s a 3953 9 uisia a U 1 5 393 i l39n39vtvln39nllle In k39 1 mm lm Concentration of ions an both sides is not equal of K Electrical potential is generated No electrical potential will be measured across PM ons move a lower Mm meme WIMWO39U 39 Equilibrlum I qmckly f cOCth O Equal concentration of K39 on Why an Electrical Potential is Generated gidc is C MampU C 14 lean3939 Side 2 is 0 Wage Kquot 7st Elsa tricoq poteh HOJ opposes 0 QO PHCL 2600 Page 1 K stops diffusing when electrical potential is equal to the force of concentration gradient 4 Why an Electrical Potential is Generated a 39 A 1 1 539 ab tea3 l 2quot can K39 maves from side 1 to side 2 taking its positive charge 39 Creation of a negatrve potential on side 1 Side 2 becomes positive relative to snde 1 Separation of charges creates an electrical potential Electrical potential opposes K39 diffusion out of the cell l 39enr not aid the opposng electrical gradient Equilibrium potential electrochemical potential generated at equilibrium can be predicted by the Nernst Equation cmsm M I mi H I H Eequiibrium potential mv R universal gas constant 831 Jmol x quotK F Faraday 96500 Coulombsmole charge T Temperature of solution 310 K I valence electrical charge 1 Simplified equation I I H I H Calculation of Equilibrium Potential Numbers represent the membrane potential at which each ion comes to equilibrium equilibrium potential for the ions for a Specific Ion Cum39mlmtimi li on intracellular Lrirarrllular Mammalian neuron l39uhhulll n Kquot 151 q Satum 1 39l l EC Uilundc IL 1 39 Q 2 5 61541 x lug mo 1 1501 90 quotiv K 1 Eh 6L5 I logquot 50o 5I 6quot HIV 9 N03 Eu6l5 I xliiglu125o 1 m39o lll39 gt Ci Many Ions Contribute to Membrane Potential It mainly depends on distribution of K39 Cl 6 Na is used to describe the membrane potential It considers concentrations of ion insideoutside cell a rmeability p of membrane to each ion PHCL 2600 Page 2 9 N05 2 Kquot cure di F eien l39 Wmugg GP 03 roe Hos gidc is I mogu c K4 leave Side 2 is 0 Wow Kquot en VS Elsatrim parish Had opposes diFmgm 16 Know hiS 1A Thesc we he PMH l icdS Cow 6L eepwmreol ion a 04 ALL ionS lrpryed W31 5 m C on PMqu mse ions Vial144 le AA ltiuA39a r3 Rule The membrane potential at any time is closest in value to the equilibrium potential for the ions to ITII UUIIIIY UI quotKHIUIWK IU CUBquot IUquot which the membrane is most permeable u H pllww w Mse ions relayViv AA sixvulgar quot MeaSW le5 Ct ox Measurement of Membrane Potential All cells in the relaxed state have a resting membrane potential lb Hananname Miaq mane tunerhm I la mum E skeletal muscle 9O mv En neuron 7O mv EmURBC 7mvto 14mv Akb cell have 0 lePCVewt eh 0 9 scamHas CV ou l ed volt6 56 Pmszu3 0 de rMiM What Do We Need to Maintain RMP Voltagegated channels are in a resting state i Emumuw tun a Paw PmllM i C ytma P 39 O 5 393 n IO a62 Okra in reg mg stock ANY domH com iA ro pCL omW ChahheAS woticing mm e cell SQ Vest How is the Resting Membrane At 70 mv resting potential K39 leaks out of the cell Cl Na is less permeable but a small amount leak into the neuron Neuron must compensate for C02 K and Na leaks Omile Na39lK ATPase maintains the resting membrane potential Trans Potential Maintained At rest the neuron is highly permeable to K 3Na outand2 K in hydrolysis of ATP Mae i4 eogs OLA Cow poured quot19 N6gt ATPOSC W16 load where toms om rom 3 N00 in 2 K out quot399 lofc N03quot is SlON Vl0U cr39 Molecwle lF gene rades Clea rmed potewHOA 399 More Lgt om one Side II HI I PHCL 2600 Page 3 o A signal which travels the length of the neuron gt During an AP the membrane potential reverses and then eventually is restored to its resting state Exchange of ions across the membrane W 7 4 1 W I r a o v Hay I quot V V g 39 k v 39 rw mu g i one 5 39 m e z i 5 I Y 15ml Characteristics of Action Potential Action potential depends on Distribution of ions Changes in membrane permeability to ions 4 Mainly Na39 and K Cl39 to a lesser degree Action of voltagegated channels o It is a shortlasting event Caused lax ion exam 5 across mem Lkmeeli ox Fed vg M 6lha a Am across can Hra 0940 m Ohlq hodeg A CF eel Ne psimm 4 4 An action potential has two main phases 1 k Reversal of polarization Membrare potential in mullwolls mV Time in milliseconds msec ThrfShoo 55 mV goes paS lquot QMP PHCL 2600 Page 4 Resting Membrane Potential quot Resting state J that y Activation 39 at39e eldse39d 4 iue l Voltagegated Na channels are in resting state Volt gated K channels are closede Na39 amp K leak channels are involved mV 70 Time gt aluminumu new gt v 00m W A qk Mmtxar a potential in mllnvollx mV Voltagegated Na channels starting to open Depolarization needs to reach a certain level or threshold 55 mv to produce an action potential Time in rnllnocmdslrmec Depolarization is a shift from the resting membrane potential toward a more positive potential Charges change across the membrane Chas 2 p images mus t weach h VEShold 0 gW l quot55 mV ole p0 Oer i zcdi Dik Generation of Action Potential MT ll 39 Reaq Nivenc om T39mhot m nun n mw autumn punMal Action potentials will have the some amplitude Independent on stimulus intensity B slkehfylln ls VClOCl39Ed tr 44 OF APS cellDays m ampM aMPHWdQ 7 kampldct c 0 id oi ADS PHCL 2600 Page 5 tnmeuuuww After the mmbrane reaches threshold Voltagegated Na chamels open Channel activation gates open Na rushes Into the neuron Building of more positive charges inside of the cell next to menialone N r Minor 1 9 39 As Membrane potential approaches 30 rnv the inactivation gate of the voltagegated Na channels closes in most channels OQC SS WW amp MKUS COIAOl quotcuDenna nirvana l o Repolarization is the process of restoring the normal resting 3 Repolarizlng phase begins Na39 channel inactivation gates close and K39 channels open Membiane starts lo become repolanzed as some K39 ions leave neuron and law negative charges begm to build up alang inSide surlace of membrane membrane potential after depolarization Na channels inactivation gate closes quot les 14 oud brings o Hgur Awnings back PHCL 2600 Page 6 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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