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Chapter 8 notes

by: Kathleen Quijada

Chapter 8 notes BME3403 EABS

Kathleen Quijada
Broward College
GPA 3.46
Engineering analysis of biological systems EABS

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Engineering analysis of biological systems EABS
Class Notes
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This 19 page Class Notes was uploaded by Kathleen Quijada on Saturday March 28, 2015. The Class Notes belongs to BME3403 EABS at Florida International University taught by Dr.Brown in Fall2015. Since its upload, it has received 50 views. For similar materials see Engineering analysis of biological systems EABS in Biomedical Sciences at Florida International University.

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Date Created: 03/28/15
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Figure ZAXOMIWSPOY or L a quot I l I I I Bunny1quot l quot COLA Cd5 Lou 109 b r V U 5 M gw m Yb pm w 09 A in cvr W r k5 5 7 1 00 2 m MKS x 39 pm 905 gm brain Nuder CS bw f f orm n btmw39er mm barmr Glial Cell Functions QK I Wg w Central nervous sysmm Support neuron bodles form myelln sheaths I my I 4 x we r 5 Barriers between compartments 1 1amp2 quot533 I 39 L 1 39 Scavengerdefense amp metabolic assrstance 1 533 Schwanncens Mfgmm Em mm Ionn l l secrete I l 1 form help form secrets take up V A 0d r Cx 39 j Supnonlor Blcc39d campanrnems Ava w WM NM 1 gm lazsrl puvb QQHMM WVAVNWH 60w 3 AULL M GUM Jiucmw WW 5 WWW p rubl my gt cn mmquotumnmg 85 Glial ccllsar 39 I quotm LN in wammm 5 my 39prerahm 3 3 MA MBquot L w W WWW W w W W N QV vaH Q9 OQ39i39DSiS NW Jl39Ccl Un Hl IMUIJarm cl died M 5 1901 9 DOCS 3 1 Y mex Electrical Signals Ionic Concentrations and Potentials Table 82 Ion Concentrations and Equllllwlum Potentials ION EXTERCELLULAR FLUID unM INTRACELLULAR FLUID lmM Eu T 37quot C K 5 mM normal range 3 55 ISO mM 90 mv Na39 HS InM normal range USHS 15 mM 60 mv amp CF 108 mM normal range lool0 to mid range SlS 63 mV m s Caquot l mM 00001 mM 522 ConccpIClieck question above 39 Membrane potential Cell concentration gradients I We ImeommmmEquilibriumMM Na ClampCa2 higher in ECF M K higher ICF Depolarization causes electrical Slgnal N tomn 5 NC d wwuXS 4 L CL U 56 g Q oh 3 Gated channels control permeability P 06 1H 014 Wm cmmisl X Lme W 0amp6 Nu 03 97 N new that V N at mo S j l e 56 0me cu bowisz mwem U l WLQ 5115 mogul but l TlUCl i Weir oQ n Jimfl N0 Qua o quotis Do metIL MA Normal 9 tom 45 W Jointr at whitii s quot 39 q e it lL 39 murd 39on UVCH U emulate withing momb rcwxe F 0quot le 01 14ch WWWS twm l h Lomee hor oPall Co Thai fits e W035 MM mamgin Vimm p rGraded Potentials Mm 3mm Ower 3m 61 Incoming signals hm MD mm a m Vary in strength i Lose strength over distance Are slower than action potentials AP r K d Pitszrnipltcneuron quot7 K i a I No generation of AP P Q quot quot f Wimp 4 339 generate AP we lay L16 1 i 39 l Figure 87 Graded potentials decrease in strength as they spread out from the point of origm lbw poiM Sum ma a2 QMH LI 8mm when 39 WM WWW tomHm ALL bf We M av 61W amp Shi hulug An OM mum rah C V Uv S wwlug quot6th af rmgw Q 339sz MT Dd bP e NClT C39Vt39tCI Mif ifQLxpencl Cm 7 Y Ma HmJL U Y QLWS 39M Pobmhal N quot UWHS Ud vodbj Su naps in3 W knivikg LDM com opw mm Chmhm quot I WA om 4 Wow 4 M 5 WC pawlMg g LWH cmmg an be LN 700m lvuh oxn j a H A CQuahbn l 1 0 OQQ L 06 W l ion 39 gt J Z 0amp0 m OWL 0 RA m to W W fwhmag 39 Rafi ch va39i if gag I V O u UN 3 U U 13 lmVOMixvl hr SECtho m Diormoms Smoa i muck M VXUh S 3WW WNW Trigger Zone Cell Intggration and Initiation of AP Trigger Zone Cell Integration and Initiation of AP a Agracled polenlial sl ans above threshold T at us initlmion polnl but decreases In strength as Ii travels through I 7 u I d me call body Al ha trigger zone R I below threshold and xhoroiore door not inimne an action polanlinl I r 39 1 1 w 2 gmquot increases i i 94 alum7x8 Hy nu poi UV 116 UNUJW39L V WW3 oi 9 I nmcxg n WM K Figure 8 811 SublImshoid and suplulhmshoid gum polemialsinuncumn Wraptroll SU m motho 0 390mm Summ Mn 39on Trigger Zone Cell Integration and Initiation of AP E Action Potential Siages Overview b A stvonger slimulu a the same point on the cell body creams a gfadea pol ntlal that 5 sun above threshold tjzy ho arm I roaches the trigger zone so an ac on pczanu ai results u g quotAll or nonequot a Signal does not diminish over distance A55 7 r 7 r r T N L 90W 1 a 39 lo DV C Krakoch l Wm Wm 9 Walme S whm witohm Mg 57 quot4 lX llqc cam l al thwart3quot 36m P fl lLeqbQ er PWWQIOQ NOD AULS Q c mRS quotI Cld imu non lAecwl VVCihdy Membrane 8 Channel Changes during an Action Potential Stages Overview Action Potential 9 5 Q l 9 g Initiation gm Depolarization 32372433339 E60 Inceaw A 39 Signal peak 9 Membrane depalanzes to lhresholct m Vollage gatedechamelsapm W e S 6 and Na eniers cell Voltagegated E Kquot channels begin to open slowly Rapid Na eniry depolarich cell Na chames close am slower K channels 0mm Resting Rising Walling Alterhyperpolarizalion Resting Action polentlal 2 3 4 Time mac 6 Kquot moves IrOm cell to extracellular l lluld 0 K channeLs remain open and additional K leaves cell hyperpolanzlng i1 ion permeabiliiy e Voltagegamd K channels close some K enlels cell lhlough leak channels l 6 Cell returns to testing ion permeability 0 39 2 3 4 l and resl39 membrane oleni al l mg n I Timemsec Figure 8339I39hc cli pnlumiul w s o in st 0 2 which con is Picailel or l Lo am C 143 lfcilcs Duh l Cg no leWa VLL Pateaha 392 mgh n39 Nxemlomm PU VLMTI39QJ a 439 39 l 0 imgnv g we ite rle lSSHl 9 7 M 7 tionl item mammals RC iu folkS m 15 h l WOW L PQXSl jaC Membrane amp Channpel Changes during an Action Regulating the AP otential a 39151 zgtmargmbmno pctentlalthe acuvauongaw C C n 1 l 2 ambn yo n bm nJZciitcl m m 9 7quot W 350 i LS no Howl MW h h me SQPCl C hm Cioh39on Pomhoi PM to Ootj39ln OJWMR A ANth ti mg Positive feedback loop l X 39 iv 5 7 393 en r 3M2 3quot 39l 5 3 35 i a Riv V A Lil l g yin1 39 1 37 Kev Figure 810 Model ol39lhc voltagegated channel Na39 Regulating the AP Regulating the AP Absolute rem 39y Relative refractory period gt pertod E36 Falling phase ji39rb 9 Action potential l IL31 E I To stop cycle 39 To gt Naquot channel l f slower Nat chantid E Na 3 gt activation gates l G FeedbaCk cyde I quotquot I inactivation gate g 39 5 Open rapid Y closes see Fig 810I 5 8 a W a E g 393 More 3 E K t v depolarization g 4 a o Zwama m lagers n V aEquot k l 2 EJEJV w leaves gt quot5 lt gt I I I I O l 2 3 Figure 81 Ion movements during the action potential Time msec q39yph39lfl u apwi r1vi m i Hi 1 ling t l nnnmmum i39upmgm VLVMV39CW WSE tlumbnr in pulill39l1m ti Hammm I39ummi39tg39 Fit3Wquot 83912 Earl me Purims lm ili Scan1amp8 Frequency of Action Potentials Frequency of Action Potentials 3 Weak stimulus releases little neurotransmitter I E 20 quot Newo lreata39issgtitter mg rate 0 int ext 31W 09444 3322 Wave ofAPs blng Mpg 0 3 gnarl g I quot 352mg Proportional neurotransmitter NT release m V 39 mma armn thllalu a Stronger GP initiates more APs amp more NT gs 2 S I l m 391 i I ALMS CutU 39 Grated Lqmcvku Ln H twm WM jg Stimunsr Receptor hr quot DY Can be MYQHcl f31 Cnltms Weinan 39 1 cam ran 6406 b7 br l qultQ UJ L W b 0 ampj V 39 1 cf A Lame vm I f quot WM Lem Conduction of Action Potentials Kinetic energy l Depolarizes ahead K Di Lil Drives AP to terminal Low cl when 3 out 3an 5 WM V1 0 A AH Tj 332316312332 V t h reaches the trigger zone channels open and Trigger zoneH Na r 39 39139 1H 0 MM ocwlwgmls bl Pr has 0t rcer Voltagegated Na Na enters the axon Conduction of Action Potentials Nit WW t gtwa A an 39w 7n uiquottt A gangli39 r twpw Jun in Wilmeru 39t39t t39amllt L m ni ign 3939Ilyquotn39l m l39quotvrrl391L39quot4ll ww Conduction of Action Potentials W open 5 more V out 9 39 39 E Che M4 S Na entry depolanzes the l I membrane which opens N m additional Nat39 channels Figure 8 113 Conduction ot nction potentials Conduction of Action Potentials rt Fmth Dc gal 1 t V or 1 n t s a39 uz39 e I Refractory region i Active regions I inactive region Na r I Na 1 1 39 1 11 Aquot777Tn 6 m 39 L 6 The trigger zone is in its refractory ltgt 39 i 6quot 0 Positive char e flows into pe md39 K 93 have 9er and In the dim pans 0 me axon J V 1 9 me Na inac va on gates have 5 4 local current ow from the 9 adiacent sections of the dosed L055 Ono from the 9 I g 9 active region causes new sectionsi axon by local current flow cytoplasm epdarizes me membrane 3 1 W of the mel39nbfar lve to depolarized Figure 814h Conduction of action potentials W Figure 814c Conduction ot39action potentials Domowre l myelin 7 quotmUH39lQLL Scar119 m CN Brani ampMD quot oquot agoc1 toms 39 lb hitii c gwmvb 5 Mods bp whim potVt 3 WM ihxgcowr pmme ww CMSS Speed of Conduction Speed of Conduction Larger diameter faster conduction TS3939S quot J S3 aquotrZ iiiy l23 axons M Nerve Axons Myelinated axon faster conduction Saltatory conduction u 3 q mjy Disease damage to myelin Chemicals that block channels Alteration of ECF ion concentrations if the 20 myelinated mammalian axons in the nerve above were each the size of a squid giant axon the nerve would have to be this size A x lt gt x L 1 gram r 39339g139 gml39rltml 1uiu In ruhInJ mg 1 litnunn quotutmme Figure 846k Axon diameter and speed ofconduction TN Laramie ortmmws 39 quot v Konj 1 TELl lnSlCL l U Weunable A ice exlmwuamr 3 Wu nbx qu gl bw P A L Speed of Conduction Cell to Cell Conduction the Synapse Node Node 0 D V an e 0 9 v N LELIN gt L I v 1 oton liftLOW l5 WWW Myanmh Example cardiac muscle am VCWW Lid IN W r wfk 7 C r n 7 u o 90 n quotIm rmdg ewh fdswu 391 it o 69 my 9 9 G Synthesis of Neurotransmitters l rotransmitters Dogma W39Wan 5m1W rC WVS myelinsneat 9W 1 cu quot emeravV m eurotransmitter receptors 394 A slows conduction n a r 2 I n 1 n r n r it 1quot 9 1quot f e e o o o e We quotUL h UQNL 1 39 1 gt If Figun SI 7 Sallalory cumluc once linokjl OLOT WOn poletrial WWquot mc f39WLhm mquot CMMS quotM WU 39Jrcrm mus 9 m F names when mm 611316 0 VLQ l rim ages 1quot allow TLC newowe e ems11 ny 47 be Vetong AZ A O W 1 V wp hxl C v gem010 ADV awnLL a WVUHtaPDmS lmka oil lieu0M6 397 w quot 39 Dhlm Simona3939 Ox NBWON ALWQL 3 O Wm 22 l hm thjon 0 A24 H 381 o n Cell to Cell Conduction the Synapse Synapse Mechanism Axon terminal An action potential depolarizes the axon terminal The depolarization opens voltage gated Cal channels and Ca2 Synaptic vesicle Mltochondrlon Axon tormlnal enters the cell Synaptic vesicles l I M 6 Calcium entry triggers exocytosis V 7 quot L 0quot 39 quot 39 of synaptic vesicle contents W n 2 s j is 903 Docking w lt PYO E m o Neurotransmitter diffuses across v the synaptic cleft and binds with I receptors on the postsynaptic cell Postsy aptic Recepwr cell 39 rquot h 1 r sites membrane 1 1 x l xtmm tquot Figure 819 Achcmical synapse quotupuuglli39 I 1 m n l dmnm m vu tlhltngul tvv1mml39trr mmr Figure 820z Events at the synapse MANWGKSW 376 0 Oilj pmml m museUs um 3 Wt Mamaea Citech hotx M Acetylcholine synthesis Neurocrines Neurotransmitters Neuromodulators Neurohormones quot1 I In t39 lftACh39 rap39dly 399 39 Q m u clu lcxlvo r3 Axon terminal Mitochondrion u39 39w g39iu g 5 de quot ouneandacetleoA Olinefgic hollne is transported back into receptor C the axon terminal and is used W to make more ACh Poslsynaptic Hm M I cell Figurth Swlhwisnndfeedingofzmt39lcholincMulesum i PM gymx3 Clgf j39yle koli nir in hibile 5 note 7 wai w I T m H7 9 Lg Meghan m way 371ro mm d 1 4L9 1 Ox 39ZOL39hOIJ imp er 1p 3 law 7 ml 14 w Cha VVzl DOEmm Camzme mof erNJ 7Z m 810 meh gym fgg39g h OrMQ C3sz View V WWH W E A lcLx01ym demure uhlnb bw 05 n he 1 1quot Mme1K Qua3m c lcgt h M h 3V n My Ere mgr C 39LUGUqJ bl cl x 4 Modem Achx nhj baked cowaf fa Sf S w imch thsf gm g L 9k5 x7lmg5 C cuim CU WVM LU bu Vb Uh maxcg 4 H Himab 227301 WW SK mea 39 3951Vampm rH e3 bi Wadtint H 0 C4M 3Vl Unixvac we incus Mgr 39 r 7 uJ P0030 SoclLUnl lt3 lymph Umam Jras re ridprior Neurocrines I Neurocrines Table 8 4 Major Neurocr lnes Table 84 Major Neurocrlnes continued KEY RECEPTOR CHEMICAL RECEPTOR TYPE39 RECEPTOR LOCATION AGONISTSIANTAGONIS ISquot MGR Acuylcholmt AClI Cholllmglc CHEMICAL RECEVI39OR TYPE RECFmR LOCATlON AGONISTSANTAGONISTSquot Nimrln rc CR Skeletal muscles Nicotineagainst Na K auxonomlc neurons CNS Guam antagonist Amino Adds Murcarinh GI CR Smooth and cardiac muscle Muscarlno agonisl Glulamah39 Giummlncrgic endocrine and exocrine nopinc anlagrmis AMPA CR Na CNS glands CNS K Amines NMDA Eire CNS a Norepinephrine NE Adrenergic GPCR Smooth and cardiac muscle u agonisr phunylephrine K car a ll endocrine and exocrine ll aniagonlsl propranoiol glands CNS it lgn yammohutyrl GABA gRCiRCI CNS Dopamme DA Dopamine Di GI CR CNS nripxyclmric drugs 39 amasomm Glycme Giycme CR Cl CNS nromocrlpnne agonisr ing Sermonln Ixhydroay Scmroncrglc ICR Na39 isquot CNS Summriplan agonlsl Mmmme plume m cpcg CNS trypramme 5HT 5HT GI CH LSD antagonist G as Histamine Histamine H Gi CR CNS Ranixidiue damn humiding mgmmgk Nlll iC oxide 340 None NM NIA wagon LUUWj 391cn 39 A orcx r 39 39 mm M lt 39 39 mm xrnelh ir I i c NR 7 I I Am 1 LI 1 c 4 39 n and Nllm nm hl lD mquot g twigs id dmhflmlfl f39 m NM dwmwk r mumm so a lywmlc and ammonium JIA a Not applicable quotquot quot 39 39 h 39 IIIm quot 39 quot quot 39 39 39 u rm 11min has rm rmludc many hcnm 4h um uc um rs Jxlrnll IlILI alllagrmnh m lilyvuluxlxdl wwurh 3an 2m mnu lm w W NhWh quott WWW rLm HP Table 344 Major Nm ncs ramm r uJl LarJm 1 Jam r1 pummel limrom39n nr Lnds Tahlc 842 Major Neumcrines Wm Ci chemois lri In rb r mv J 0 pam Sirrnoloklrf 4 1quot on Jenquothigh Multiple Receptors modify signal Multiple Receptors modify signal i tiblw39nc Nm omN Ng wyfarwg 30 CA i Slow synaptic potmllals 39 a v Shani an I n I gt w fas swapquot pawns o turoimnsmrgot and longterm e ecis L o Chemacally 39 G pram 11mm 4 gated Ion channel mceoior ML 39 F3 I channei opening 3 QM PVNHS39LOLOCJV r I Slow protein synthesis m2 1 1 39 Duration a i 5 AP A ANGIE open state 039 ion channel 5 V i iW Jr ule lasing Jr UNNCJQ 511mm obi 3n W cm M Di Rb ij Whiting WU KR Jrx S ro 1A Mmaimrxc n purgmi IvumpmMumm b1 lmlvinrl ingu litmunmi rlmnlug39i quotmu5 Inactivation of Neurotransmitters ELLWWM be Recycled ififgg limflzl l ilii Enzyme degradation Diffuse away Synaptic vesiCIe j Enzymes inactivate l neurotransmitters a Neurotransmitters can diffuse I out of the synaptic cleft x 39 39 IOKLLlezlw Nb gag4amp5 it My 5 Wuer ll Meryl CVmHNW bL quot awlwre 4 Chem W l39t f b towl Emt9 39NT39i W hl W 3 w S clmrt39n WL or U9 n m W1 p cn39rltc w Integration Of Signals 2 p quotBumquot brancmsma w Information transfer at each exchange 5g Signal can be lost my Signal can be enhanced ow one cell to many l l l i 3quot iii l igurt 8 24quot Convergence and divergence brig Qr ydQ ph newom W cm 0N g h a ed a la my 7 d 3 0 1rsv1 Motto MC QtW V13 M PNSynap L NJWOYW mnwgrt m Hutnu at gmth all or PbgtS39ynqph UN y presynaptic neurons converge to m i quotn stsynaptic neurons Convergent Integration Additive Summation 0 Multiple excitatory GPs Temporal summation Additive strength at trigger zone lidUK 0 ll W RHck Oil lm i ii a we WM 9 armhquot a lieUH uot r pom r71 OilWM 10W botud Axon terminals Dendrile of of presynaptic postsynaptic Dendrite Glial cell processes 1 para n l39rUvnl39xJuuumI 1m hm n l cunnmw mmm Figum 804w Convergence and divergence n MY O Figure 25 Inculiuns of on a postspmptic neuron l SPQ al Sbmmmhbn l Presynaptic 39 axon terminal 5 Three excitatory neurons fire Their graded potentials separately are all below threshold w l S orH Al Sumrncri b e Graded potentials arrive at trigger zone together and sum to create asuprathreshold Signal 0 An action potential IS generated ll gr 1M 0th polemm potential or m 5 03m LilmvkelS Figure 8 26u Spatial summariun Tl t wimp pOtcm dl COM NonCl 1 QLLRCmnL spews 04 W V fLlu whim3 b alignwny Mi mqmmtma com mm taier blow MA st itstwice Convergent Integration Inhibitory Nervous Tissue Development Surnmatigri 100 billion neurons find their target inhibitory GPs I Growth cones cance v strength of Follow growth factors structural proteins excitatory GP Neurotropic factors sustain new synapse 39 Signal at quotUse it or loose itquot men is enerae weak no AP produced l igurc 26 Spatial summation The brain corms H r 9 wCCKS Erma Colinha 394Fl Cam e m m wbv m Lactic o imiqu FK H bikii 1C0l 5 4quot 1 mwmplq oh m Cx pctrm OVCL Pathologies Pathologies no Drugs in ECF L i if r iwgg a wax 7 f yew Disorders of ion balance 9quot 39 Too muchtoo little NT release V3 1394 I Examples Parkinson39s schizophrenia epilepsy 1 depression C lawn 0 WD tramsmillu Limited regrowth Parallel nerves help some Figun 8 31Injurym neurons Summary Organization and role of the nervous system CNS amp components of PMS Neuron and glial cell structure and function Electrical signals from waves of depolarization Graded potentials function and mechanism Action potentials function and mechanism Synapse neurotransmitters cell to cell communication Conduction integration and modulation of the signals Development and pathologies of the nervous system


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