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Skeletal muscle structure. striated long multinucleate cells extend from tendon to tendon formed by fusion of myoblasts innervated by somatic nervous system one neuromuscular junction per fiber cardiac & smooth muscle later. fig 9-1a. Skeletal muscle structure. fig 9-2.
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Skeletal muscle structure striated long multinucleate cells extend from tendon to tendon formed by fusion of myoblasts innervated by somatic nervous system one neuromuscular junction per fiber cardiac & smooth muscle later fig 9-1a
Skeletal muscle structure fig 9-2
Skeletal muscle structure fig 9-2
Skeletal muscle structure fig 9-3 Don’t bother with: I band, A band, H zone, M line
Skeletal muscle structure 6 thin filaments around each thick 3 thick filaments around each thin fig 9-4
Neuromuscular junction fig 9-14a
Neuromuscular junction fig 9-14b
Generation of motor end plate potential (notes) action potential in somatic motor neuron depolarization of axon terminal, opening of voltage gated Ca++ channels Ca++ enters cell & activates fusion of AcCh vesicles with docking sites AcCh released into synaptic cleft AcCh binds to non-specific ligand gated cation channels in motor end plate opening of channels; Na+ influx greater than K+ efflux motor end plate potential occurs (EPSP) & spreads to edge of plate edge of motor end plate acts like initial segment of axon terminal voltage gated Na+ & K+ channels generate action potential in muscle note: motor nerve action potential always generates muscle action potential Relaxation: AcCh release ends; acetylcholinesterase hydrolyses AcCh; choline transported back into axon terminal
Structure of sarcoplasmic reticulum fig 9-11a
Structure of sarcoplasmic reticulum fig 9-11b
Ca++ release from sarcoplasmic reticulum (s.r.) fig 9-15 cropped action potential spreads across muscle membrane and down T tubules depolarization sensed by dihydropyridine (DHP) receptor in T tubule wall DHP receptor opens ryanodine receptor & its Ca++ channel in s.r. wall Ca++ released into cytosol; subsequently returned to s.r. by Ca++ ATPase
Interaction of thick and thin filaments fig 9-07a Myosin cross bridges bind to sites on actin (when exposed)
Myosin structure fig 9-07b Heavy chains (paired): tail, hinge & cross bridge Light chains (2 pairs): involved in ATPase activity & regulation
Ca++ binds to troponin fig 9-12 Ca++ binds to troponin which causes tropomyosin to move to side exposed sites on actin bind/release myosin cross bridges
Troponin function: low Ca++ fig 9-9a in absence of Ca++: troponin holds tropomyosin against cross-bridge binding site on actin
Troponin function: high Ca++ fig 9-9b in presence of Ca++: troponin moves tropomyosin away from cross-bridge binding site on actin
Cross bridge cycling (notes) Resting state [Ca++], X-bridge binding site covered X-bridge energized (A + *MADPPi) Ca++ release from s.r. [Ca++] exposes X-bridge binding site on actin energized X-bridge binds to actin, ADP & Pi released (step 1) X-bridge “uncocks” as thick filament slides past thin filament (AM) (step 2) ATP gets involved ATP binds to myosin, releasing actin binding (MATP + A) (step 3) X-bridge is energized (cocked) MATP *MADPPi (step 4) Cycling continues until [Ca++] falls
Muscle relaxation action potentials in motor nerve cease AcCh in synaptic cleft hydrolyzed by acetylcholinesterase action potentials in muscle fiber cease Ca++ pumped back into sarcoplasmic reticulum troponin moves tropomyosin to cover X-bridge binding sites myosin remains in *MADPPi form antagonistic muscle extends relaxed muscle
Muscle fiber contraction fig 9-10 This is the response of a single muscle fiber to a single action potential