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Week 2 of Reading Notes

by: Muni Notetaker

Week 2 of Reading Notes Bio Sci E109

Muni Notetaker
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Lecture 5 Lecture 6 Lecture 7
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This 14 page Class Notes was uploaded by Muni Notetaker on Sunday October 11, 2015. The Class Notes belongs to Bio Sci E109 at University of California - Irvine taught by LOUDON, C. in Summer 2015. Since its upload, it has received 53 views. For similar materials see HUMAN PHYSIOLOGY in Biology at University of California - Irvine.

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Date Created: 10/11/15
Lecture 5 Sunday ct ber 4 2 15 82 1 PM Chapter 1 Cellular Physiology Action Potentials Excitable cells such as nerve and muscle consist of a rapid depolarization upstroke followed by repolarization of the membrane potential Basic mechanism for transmission of information in the nervous system and all types of muscle Terminology O 0000 Depolarization process of making the membrane potential less negative on the interior of the cell It can all cause it to become more positive Hyperpolarization process of making the membrane potential more negative Inward current ow of positive charge into the cell depolarizing the membrane potential Outward current ow of positive charge out of the cell hyperpolarize the membrane potential Threshold potential membrane potential at which occurrence of the action potential is inevitable 39 Threshold is less negative than the rest of the membrane potential therefore an inward current is required to depolarize the membrane potential to threshold 39 Net inward current becomes larger than outward current and the resulting depolarization becomes selfsustaining therefore giving rise to action potential 39 Net inward current is smaller than outward current than membrane will not depolarized to threshold and action potential will not occur Overshoot portion of the action potential where the membrane potential is positive Undershoot also known as hyperpolarizing after potential portion of the action potential following repolarization where the membrane potential is actually more negative than it is at rest Refractory period period during which another normal action potential cannot be elicit in an excitable cell Characteristics of Action Potential 0 Stereotypical size and shape normal action potential looks identical for a given cell type depolarizes to the same potential and back to the same resting potential Propagation action potential at one site causes depolarization at adjacent sites bringing those adjacent sites to threshold 39 Nondecremental propagation of action potentials from one site to the next Allornone response action potential either occurs or not 39 If excitable cell is depolarized to threshold in normal manner the action potential occurs 39 If membrane is not depolarized to threshold action potential does not occur however if stimulus is applied during refractory period then action potential occurs without stereotypical size and shape or does not occur Ionic Basis of the Action Potential Reading Notes Page 1 Imam rI el r 211 Kill1m mm Farms 433 m Hm MIME f major nilEzul l Eff f i 5 i F i r r V Hi 39 Ii Ill g ll39l39lllllr uh I39 i HI HF u quot l l A E if i391 Fi If U quot I I all I l iii E H l1 i gulp 1e LE E if a sip a H IVIIZEII39TEEIEIJI39HIJP In in illL Elli m V l 39II I 53 En 3 33 m 39 35 3Liim1 quotFquot i quot a Jquot In nh k lial 35 llTL39iir quot E1 WMM Manual I I 1ZI 1 Tum lillrlll ieli illi39l39msli i ii potential 2 Upstroke of the action potential inward current causes depolarization of the nerve cell membrane to l Resting membrane potential membrane potential is 70mV at rest K conductance or permeability is high therefore allowing the diffusion of K ions out of the cell and down the concentration gradient This diffusion creates K diffusion potential which drives membrane potential towards the K equilibrium potential At rest Na conductance is low therefore resting membrane potential is far from Na equilibrium threshold occurs at 60mV i This causes rapid opening of activation gates of the Na channel and conductance increase becoming higher than K resulting in inward current Tetrodotoxin and lidocaine block the Na channels preventing occurrence of action potential i1 3 Repolarization of the action potential upstroke is terminated and the membrane potential repolarizes to the resting level This occurs because the inactivation gates of Na channels respond to depolarization by closing but i its slower than activation gates Therefore after the delay the inactivation gates close the Na channels terminating the upstroke ii Depolarization opens K channels increasing its conductance higher than Na which results in an outward K current and the membrane is repolarized Tetraethylammonium TEA blocks voltagegated K channels 111 than at rest and membrane potential is driven closer to K equilibrium potential When K returns to rest membrane potential depolarizes slightly back to resting potential and the 4 Hyperpolarizing afterpotential undershoot following repolarization the K conductance is higher i membrane is now ready to be stimulated to generate action potential The Nerve Na Channel 0 Voltagegated Na channel is an integral protein that is responsible for the upstroke of the action potential 39 Consist of a large 0 subunit and two 3 subunits 39 0t subunit has 4 domains which has 6 transmembrane Othelices which surround a pore that allow the ow of Na ions Reading Notes Page 2 39 Response to depolarization MiraJilin mini 1 At rest activation gate is closed therefore Na cannot ow through despite inactivation gate being open 2 During upstroke of the action potential depolarization to threshold causes activation gate to open therefore brie y allowing Na ions to ow through 3 At peak of action potential the inactivation has a delayed response and closes and repolarization begins until it reaches resting level therefore closing activation gate and opening inactivation gate Refractory Periods O Excitable cells are incapable of producing normal action potentials Absolute Refractory Period 39 Overlaps with almost the entire duration of the action potential during this time another action potential cannot be elicited 39 Provides closure of the inactivation gates of the Na channel in response to depolarization Relative Refractory Period 39 Begins at the end of the absolute refractory period and overlaps primarily with the priod of hyperpolarizing afterpotential and during this time an action potential can be elicited 39 Inward current is needed to bring the membrane to threshold for the next action potential because membrane potential is closer to the K equilibrium potential Accommodation 39 When the threshold potential may pass without an action potential having been fired occurs due to depolarization which closes inactivation gates on the Na channels III Ex hyperkalemia people with elevated serum K concentration Propagation of Action Potentials O Occurs by the spread of local currents from active regions to adjacent inactive regions Reading Notes Page 3 Mtggala mun 39 A initial segment of the nerve axon is depolarized to threshold and res an action potential The polarity is then reversed due to the inward Na current causing the cell interior to be positive The adjacent region remains negative 39 B at the active site positive charges inside the cell ow toward negative charges at the adjacent inactive sire causing the adjacent region to depolarize to threshold 39 C adjacent region of the axon res action potential Polarity of the membrane potential is reversed and the inside of the cell becomes positives while the active region is repolarized back to resting membrane potential and the cell is negative inside Changes in Conduction Velocity 39 Two mechanisms that increase velocity along a nerve 1 Increasing nerve diameter internal resistance Ri is inversely proportional to the cross sectional area therefore the larger the ber the lower the Ri Length constant is inversely proportional to the square root of Ri therefore when length constant is large when Ri is small The largest nerves have the longest length constant current spreads farthest 2 Myelination Myelin is a lipid insulator of nerve axons that increases Rm and decreases Cm a Increased Rm current ows along the path of least resistance of the axon interior rather than across the high resistance path of the axonal membrane b Decreased Cm produces a decrease in time constant therefore at breaks in myelin sheath the axonal membrane depolarizes faster in response to inward current 39 Nodes of Ranvier breaks in the myelin sheath causing there to be low Rm and current can ow across the membrane and action potentials can occur III Saltatory conduction action potentials quotjumpquot long distances from one node to the next Synaptic and Neuromuscular Transmission Synapse site where information is transmitted from one cell to another either electrically or via chemical transmitter Types of Synapses Electrical Synapses 39 Allow current to ow from one excitable cell to the next via low resistance pathways between the cells called gap junctions El Account for very fast conduction in cardiac muscle and some types of smooth muscle tissue Chemical Synapses Reading Notes Page 4 39 Gap between the presynaptic cell membrane and the postsynaptic cell membrane called the synaptic cleft 39 Information is transmitted across the synaptic cleft via neurotransmitters a substance that is release from the presynaptic terminal and binds to receptors on the postsynaptic terminal 39 Unidirectional from presynaptic to postsynaptic 39 Synaptic delay time required for the multiple steps in chemical neurotransmission to occur Neuromuscular Junction Example of a Chemical Synapse Motor Units 39 Motoneurons nerves the innervate muscle bers 39 Motor unit single motoneuron and muscle ber innervates it Sequence of Events at the Neuromuscular Junction 39 Neuromuscular junction synapse between a motoneuron and muscle ber H THEU ii HUSELE Fma lmp a innma tar minai HE EVEEl Ei EEI Hf Il mumr 1 mm WEE I39HJEI 39 J9 WE Hil 39lilflilii iii i ifl if EITEE39ETHFJ39TEZ ETITIIIliiilL E39 li i li i l LEIquot WEE WEHTI EWIJ Jl f i m ags iai39laa39lriala and Ira Ina ma immili39lal a AEE ti iIri tlillnEI iiiam I5 aim ma a39yrriapaa an aim J Ii Mi i IEIIFiIZJE ITEI TEES I39IZ IZEI ZIEDI iii m bl i and Ham 5 EI39TIEIE39il39i E F l Pia39 arid lEZ39 El DEERE m iiia mama arm tiara a WWI l i l l i a1 aria mainr anal plaia mnaaa amlmi mmmlaia in ganaraiam in limit adjEmmi FiTIIJEZIIZ39 IISELLEE Equot IELIEI TI E degraded m EWWE and ll11mm Wai 39 V IJITEIEI39 L CI iEi ia iaizan ham Iran iina iiraaymaaitia ianmmai an an iiamlmllma miraaamriai Agents That Alter Neuromuscular Function REFINE A a ti g Hummuaamar Tra amlasmn Eaamaiia Marian Hiram ma Hm39iamalar iiaifiiliimla imam Email Nauaiigmiim Halalit39haiiiiiiinri ilaalliza i ii h ralaa aa Tram pmayaanizia Tana hinalaadia pmaliiaiia rilf iEanairaiaaa mliaclmi aaii iarminraia riaailii lampEma ariiii fair maepima an aaraaaaa aiaa if EFF in mamimai adaaaa familiaaa riluiur and malaria paraiiiiraia impiraiimy unilaialea and milli MIhE iliiiihiim aititzlfiuliiaaiiaraaej FILill g and eerllliarlima airtiml Ui iiijiil an Initial and plantar Iiiluiiiia maintakie iii ulalinra iillli Depeiaa l aiurea iIIL39II1 praayanaptii ian39iiinail meay39iiapiia terminal sti ing Metalsingling hEhE aaaiyrlKril Ialii laalaraaa EPE and plain platanimal Types of Synaptic Arrangements 0 Onetoone synapses a single action potential in the presynaptic cell the motoneuron causes a single action potential in the postsynaptic cell the muscle ber 0 Onetomany synapses an action potential in the presynaptic cell the motoneuron causes a burst of Reading Notes Page 5 action potentials in the postsynaptic cells causes ampli cation of activity 0 Manytoone synapses action potential in the presynaptic cell is insuf cient to produce an action potential in the postsynaptic cell therefore many presynaptic cells converge on the postsynaptic cell and the inputs determine whether the postsynaptic cell will re an action potential Synaptic Input Excitatory and Inhibitory Postsynaptic Potentials O The manytoone synaptic arrangement is a common con guration in which many presynaptic cells converge on a single postsynaptic cell with inputs being either excitatory or inhibitory Excitatory Postsynaptic Potentials 39 EPSPs are synaptic inputs that depolarize the postsynaptic cell bringing the membrane potential closer to threshold and closer to ring an action potential 39 Produced by opening Na and K channels Inhibitory Postsynaptic Potentials 39 IPSPs are synaptic inputs that hyperpolarize the postsynaptic cell taking the membrane potential away from the threshold and farther from ring an action potential 39 Produced by opening Cl channels Integration of Synaptic Information 0 Presynaptic information that arrives at the synapse can be integrated in two ways Spatial Summation 39 Occurs when two or more presynaptic inputs arrive at a postsynaptic cell simultaneously 39 If they are both excitatory they combine to create a greater depolarization if one of them is excitatory they cancel each other out 39 Can occur when inputs are far apart as well Temporal Summation 39 Two presynaptic inputs arrive at the postsynaptic cell in rapid succession Other Phenomena That Alter Synaptic Activity 39 Facilitation augmentation and posttetanic potentiation repeated stimulus causes the response of the postsynaptic cell to be greater than expected by an increased release of neurotransmitters into the synapse by accumulation of Ca2 in presynaptic terminal 39 Longterm potential occurs in storage of memories and involves increased release of neurotransmitters from presynaptic terminals and increased sensitivity of postsynaptic membranes to the transmitter 39 Synaptic fatigue occur where repeated stimulus produces a smaller than expected response in the postsynaptic cell resulting from depletion of neurotransmitter stores from the presynaptic terminal Neurotransmitters 0 Transmission of information at chemical synapses involves the release of a neurotransmitter from a presynaptic cell diffusion across the synaptic cleft and binding of the neurotransmitter to speci c receptors on the postsynaptic membrane to produce a change in membrane potential Acetylcholine 39 Ach is the only neurotransmitter that is utilized at the neuromuscular junction 39 Released from all preganglionic and most postganglionic neurons in the parasympathetic nervous system and from all preganglionic neurons in the sympathetic nervous system 39 Released from presynaptic neurons of the adrenal medulla ll 7 a H Choline and acetyl CoA combine to form ACh Reading Notes Page 6 39 Released from presynaptic neurons of the adrenal medulla if Choline and acetyl CoA combine to form ACh Eh lm newi an wh1ch 1s catalyzed by choline acetyltransferase Ey hgg mammgm g Ach is released from presynaptic nerve terminal and diffuses into postsynaptic membrane where ngpi kg it binds and activates nicotinic ACh receptors AChE degrades ACh to choline and acetate i which terminates the action of ACh at the agrantHm WWWE39 postsynaptic membrane 12 of the choline is taken back into presynaptic terminal to be quotEmma Ema reutilized for synthesis Reading Notes Page 7 Lecture 6 Tuesday ct ber 6 2 15 622 PM Chapter 1 Cellular Physiology Skeletal Muscle Excitationcontraction coupling events that occur between the action potential in the muscle ber and contraction of the muscle ber Muscle Filaments 0 Each muscle ber behaves as a single unit multinucleate and contains myo brils 39 Myo brils are surrounded by sarcoplasmic reticulum and are invaginated by transverse tubules Think laments Thin MamEH11 ErmaSin arming tropomyosin mpnnim Tail Trmp mwsir Thick Filament 39 Comprised of III Myosin large molecular weight protein that has 6 polypeptide chains 1 pair of heavy chains and 2 pair of light chains III Heavy chains have a helical structure forming the tail III The four light chains form the globular head which have actinbinding site Thin Filaments 39 Composed of three proteins III Actin Globular protein called G actin Polymerized into two strands that twist into a helical structure to form lamentous action F actin Contains myosinbinding sites III Tropomyosin lamentous protein that runs along the groove of each twisted actin lament Function is to block the myosinbinding site when at rest III Troponin complex of three globular proteins troponin T troponin I and troponin C located along intervals of the tropomyosin lament Troponin T attaches troponin to tropomyosin Troponin I inhibits the interaction of action and myosin by covering the myosinbinding site Troponin C Ca2 binding protein plays role in initiation of contraction 0 Intracellular Ca2 increases Ca2 binds to troponin C producing functional change in troponin complex which moves tropomyosin out of the way permitting the binding of actin Arrangement of Thick and Thin Filaments in Sarcomeres Reading Notes Page 1 m1 Illaamend F 11mm Manama qu g g 5 mgff y u z x jf cL H Era I 2 2 14quot 3 r 7 L m w 71 39 39 knja n i Ej u t n j 7 it 1 r r 1 712 ztxzxigzvrgzyrgi zgmrxzx i3 EEK 1 i1 139 as i1 1 FG 7 a I2 1quot La arr K a E n bland ll Jami M 33mm 39 Sarcomere basic contractile unit that is delineated by the Z disks III Each contains a full A band in the center and 12 of 2 I bands on either side of the A band 39 A bands located in the center contain thick laments that appear dark under polarized light III Can be overlapping of thick and thin filaments resulting in sites for crossbridge formation 39 I bands located on either side of A bands appear light under polarized light III Contain thin filaments intermediate filamentous proteins and Z disks III No thick laments 39 Z disks darkly staining structure that runs down the middle of I bands 39 Bare zone located in center of each sarcomere and contains no thin filaments or thick filaments 39 M line bisects the bare zone and contains darkly staining proteins the link central portions of thick filaments together Cytoskeletal Proteins 39 Establish the structure of myofibrils ensuring the thick and thin filaments are aligned correctly and at proper distances from one another 39 Transverse CP link thick and thin filaments forming a scaffold for myofibrils and linking sarcomeres of adjacent myofibrils 39 Dystrophin an actin binding protein that anchors entire myofibril array to cell membrane 39 Longitudinal CP includes titin and nebulin proteins III Titin associated with thick filaments extends from M lines to Z disks Part of it passes through the thick filament and the rest is elastic which is anchored to Z disk The elastic portion changes as sarcomere length changes Helps center the thick filament in the sarcomere III Nebulin associated with thin filament single nebulin extends from one end of the thin filament to the other and serves as a quotmolecular rulerquot III a Actinin anchors the thin filament to Z disk Transverse Tubules and Sarcoplasmic Reticulum 39 Transverse T tubules extensive network of muscle cell membrane that invaginates deep into the muscle fiber III Carries depolarization from action potentials at the muscle cell surface to the interior of the fiber III Dthydropyridine receptor a voltage sensitive protein that is in the terminal cisternae of the sarcoplasmic reticulum with which T tubules make contact with 39 Sarcoplasmic reticulum internal tubular structure that stores and releases Ca2 for excitationcontraction coupling III Contains a Ca2 release channel called ryanodine receptor 39 Ca2 ATPase SERCA Ca2 accumulation in the sarcoplasmic reticulum III Pumps Ca2 from ICF of the muscle fiber into the interior of the sarcoplasmic reticulum keeping intracellular Ca2 low when the muscle fiber is at rest III Calsequestrin low affinity high capacity Ca2 binding protein Helps main low levels of Ca2 in the SR Reading Notes Page 2 ExcitationContraction Coupling in Skeletal Muscle O a mechanism that translates the muscle action potential into the production of tension 0 Temporal relationships are critical in that the action potential always precedes the rise in intracellular Ca2 concentration which always precedes contraction 0 Steps EEGI I ITI39IEIH IIE39I39 FMI2quotI391III H IHKEi El ETM HUBBLE Mllen mnlnl m mach manMm I e an mwmn m 139 runs a rareom 5 915 mkm wna n ii39il 39snulmr i m j T 1quot 39l lmsmi ar I139quot minim E as hmlrszpmij J 39I Iwgmn mu ar ulnas HelmquotJam Ilzijn 3111 magiu E Earning and mmraim w IiiBF l ifELI39E39UELL39EU Ezra Ir rutImamquot 0 Cross Bridge Cycling Position of Actln and Myosin Durlng Crossbrldge Cycllng Actm filament e r G Myosnn head Myosm tulamom O A D B 9 C 9 D e L A 1 Action potentials in muscle cell membrane are propagated to the T tubules 2 Depolarization of the T tubules causes conformational change in voltagesensitive dihydropyridine receptors Ca2 channels are opened 3 Increase in intracellular Ca2 concentration 4 Ca2 binds to troponin C on the thin filaments causing conformational change in the troponin complex 5 Conformational change causes tropomyosin to be moved out of the way so that crossbridge cycling can begin 6 Cross bridge cycling and the formation of bridges is associated with generation of force 7 Relaxation occurs when Ca2 is reaccumulated in the SR by Ca2 ATPase Events ATPADP Rugor No nucleohdes bound ATP binds to cleft on myosun head Conformational change so myosm AT P bound Decreased amnny of myosan tor actin Myosin released Cleft closes around ATP Contormatronal change M p ADP p39 Myosin head displaced toward G end ADP p bound 0 actin ATP hydrotyss Myosm head bonds new site on actin ADP bound Power stroke loroe ADP released Reading Notes Page 3 1 2 3 4 5 No ATP is bound to myosin which is tightly attached to actin in a quotrigorquot position The binding of the ATP to a cleft produces conformational change in myosin which decrease affinity of actin Cleft encloses the ATP molecules producing further conformational change which causes myosin to be displace toward positive end of actin and ATP is hydrolyzed Myosin binds to new site on actin constituting the force generating power stroke Each cross bridge cycle walks 10 nanometers along actin filament ADP is released and myosin returns to original position original position ADP released No DUCIGOHdeS bound Rigor E Mechanism of Tetanus 0 Single action potential results in the release of a xed amount of Ca2 from the SR to produce a single twitch 39 Twitch is terminated when SR reaccumulates Ca2 39 How stimulus of the muscle can cause there to be insuffient time for reaccumulation of Ca2 this results in continuous binding of Ca2 to troponin C and a tetanus contraction occurs LengthTension Relationship 0 Refers to the effect of muscle fiber length on the amount of tension the fiber can develop 0 Isometric contraction muscle allowed to develop tension at a preset length called preload but it not allowed to shorten 39 Passive tension tension developed by simply stretching a muscle to different lengths 39 Total tension tension developed when a muscle is stimulated to contract at different preloads The sum of active tension and passive tension 39 Active tension determined by subtracting the passive tension from the total tensions represents the active force developed during crossbridge cycling 0 Unusual relationship between active tension and muscle length 0 Active tension developed is proportional to the number of crossbridge that cycle therefore active tension is maximal when there is a maximal overlap of thick and thin filaments and possible crossbridges 39 When muscle is stretched to longer lengths less crossbridges and active tension reduced and vice versa TE Si CH1 quot x Length at maximum my a crusabridgre overlap N m Muscle length or preload Force Velocity Relationship 0 Describes the velocity of shortening when the force against which the muscle contracts the afterload is varied Determined by allowing the muscle to shorten Isotonic contraction force is fixed rather than length Speed of crossbridge cycling shown by velocity of shortening When the afterload on the muscle is zero the velocity of shortening is at Vmax 00000 When afterload is increased velocity is decreased towards zero Reading Notes Page 4 Reading Notes Page 5 Lecture 7 Menday cteber 12 2 15 938 AM IChapter 1 Cellular Physiology Smooth Muscle Lacks striations therefore distinguishes it from skeletal and cardiac muscle 0 Striations are made of thin and thick laments in sarcomeres but in smooth muscle striations lack because the thin and thick laments are not organized in sarcomeres Founds in walls of hollow organs gastrointestinal tract bladder the uterus Functions 0 To produce motility and to maintain tension Types of Smooth Muscle O Classi ed as multiunit or unitary depending on whether they are electrically coupled or not 39 Unitary smooth muscle have gap junctions between cells which allow for fast spread of electrical activity throughout the organ followed by coordinated contraction 39 Multiunit smooth muscle has little or no coupling between cell 39 Combined smooth muscle only found in vascular smooth muscle Unitary Smooth Muscle 39 Present in gastrointestinal tract bladder uterus and ureter 39 Contract in coordinated fashion due to cells that are linked by gap junctions III Low resistance pathways for current ow which permits electrical coupling between cells 39 Slow waves spontaneous pacemaker activity also characterizes the unitary smooth muscle III Frequency of waves sets characteristic pattern of action potentials within an organ this then determines the frequency of contractions Multiunit Smooth Muscle 39 Present in the iris the ciliary muscles of the lens and the vas deferens 39 Each muscle ber behaves as a separate motor unit and there is little to no coupling between cells 39 Densely innervated by postganglionic bers of the parasympathetic and sympathetic nervous systems which regulate function ExcitationContraction Coupling in Smooth Muscle 0 There is troponin so the interaction of actin and myosin is controlled by the binding of Ca2 to another protein called calmodulin which regulates myosinlightchain kinase and regulates crossbridge cycling Mechanisms that Increase Intracellular Ca2 Concentration in Smooth Muscle HMSEEE EELL H HumaneEur 51 7 gt quot 7 a Ca agrant Reading Notes Page 1 iglLLiETEUE SELL HormoneDr FITIEELII39EIEIE39I Ermltar I quot i F5 Ea wattageWM A Ea channel uprna l dl Ea hannal A i Home Izir TiEli Elf I1 ii i i l f a mplasmilz reli llur m nah ILiglandigial Iad Gait Iihannra 39 Voltagegated Ca2 channels sarcolemmal Ca2 channels that open when the cell membrane potential depolarizes This allows action potentials in SM to cause voltage gated Ca2 channels to open allowing the ow of Ca2 into the cell down electrochemical gradient 39 Ligandgated Ca2 channels regulated by receptormediated events III Various hormones or neurotransmitters interact with speci c receptors in the sarcolemmal membrane which are couples Via GTPbinding protein to the Ca2 channels When the channel opens Ca2 ows into the cell 39 IP3gated Ca2 channels present in sarcoplasmic reticulum membrane rather than ECF III Hormones or neurotransmitters interact with speci c receptors on the sarcolemmal membrane which are coupled Via GTPbinding protein to phospholipase C Phospholipase C catalyzes hydrolysis of PIP2 to 1P3 and DAG III 1P3 diffuses into sarcoplasmic reticulum where Ca2 is released which channels owing from storage sites into ICF Reading Notes Page 2


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