Chapter 9.2 Cheat Sheet (DRAFT) by jjovann

•In order for contra­ction of skeletal muscle to occur, electrical signals (action potent­ials) from motor neurons must be transf­ormed into chemical signals (neuro­tra­nsm­itters)
–Takes place at the neurom­uscular junction
•These chemical signals then stimulate electrical signals in sarcolemma of the muscle fiber - if the chemical stimul­ation is strong enough.
•The electrical signal in the muscle fiber (action potential) then activate a series of events that lead to the shortening of the skeletal muscle fiber

•Predo­minant theory of skeletal muscle contra­cti­on–Well supported by research
•Sliding filament model of contra­cti­on–­Int­era­ctions between the thin and thick filaments of the sarcomere produce the contra­ction (short­ening) of a skeletal muscle cell
–In relaxed state, thin and thick filaments overlap slightly
–During contra­ction, thin filaments slide toward the m-line past the thick filaments actin and myosin overlap more
•Occurs when myosin heads bind to actin and pull cross bridges and power stroke

•Brief overview of action potential (AP)–AP dependent on voltage gated Na+ and K+ channel intera­ctions
–Normal resting membrane voltage
•There is a difference in charges inside the cell vs outside –Inside charge is negative compared to outside (outside value is 0)
•Na+ at high concen­tration outside the cell vs inside•K+ at high concen­tration inside the cell vs outside

•Events that transmit AP along sarcolemma lead to sliding of myofil­aments
•AP brief; ends before contra­ction
–However, causes rise in intrac­ellular Ca2+c­ont­raction
•Latent period
–Time when E-C coupling events occur
–Time between AP initiation and beginning of contra­ction

•Depol­ari­zat­ion­phase - generation and propag­ation of an action potential (AP)
–End plate potential spreads to adjacent membrane areas
–Volta­ge-­gated Na+ channels open–Na+ influx decreases membrane voltage (makes less negative) toward critical voltage called threshold
•Membrane voltage in which AP will begin
–If threshold reached, AP initiated
•Rapid increase in amount of open voltage gated sodium channels
•Rapid Na+ influx into the cell leads to fast positive change in voltage of the intrac­ellular side of membrane
•Na+ flows into the cell, down its electr­och­emical gradient
–Once initiated, is unstop­pable muscle fiber contra­ction

•Situated midway along length of muscle fiber
•Axon terminal and muscle fiber separated by gel-filled space called synaptic cleft
•Synaptic vesicles of axon terminal contain neurot­ran­smitter acetyl­choline (ACh)
•Junct­ional folds of sarcolemma contain ACh receptors
–nAChR (nicotinic acetyl­choline receptor)
•NMJ includes axon terminals, synaptic cleft, junctional folds

•Chemical gradients of skeletal muscle at rest–C­omp­arison intrac­ellular [X] vs. extrac­ellular [X] (Sarco­plasmic vs. inters­titial)
•Intra­cel­lular [Ca] very low•In­tra­cel­lular [Na] very low
•Intra­cel­lular [K] high
•At rest, the average skeletal muscle cell internal membrane voltage (charge at the surface of the intrac­ellular portion of the plasma membrane) is -95mV with respect to a 0 mV outside membrane voltage
–The charge at the surface of the extrac­ellular side of the membrane is almost always 0mV

•Generic graphic for a skeletal muscle cell
–Compares membrane voltage and concen­tra­tions of important ions inside vs. outside

•Nerve impulse arrives at axon terminal  ACh released into synaptic cleft
•ACh diffuses across cleft (from high concen­tration to low) and binds with ACh receptors on sarcolemma 
•Elect­rical events  generation of action potential

•Resting sarcolemma polarized
–Voltage across membrane different
•Action potential in sarcolemma caused by changes in electrical charges
•Occurs in three steps
–End plate potential
–Depol­ari­zation
–Repol­ari­zation

•AP spreads across sarcolemma •Volt­age­-gated Na+ channels open in adjacent sarcolemma portions causing them to depolarize to threshold
–Spreads across sarcolemma very quickly

•AP propagated along the sarcollema and into T-tubules
•AP travels down into the T-tubules where it activates DHP receptors
•DHP receptors
–These voltag­e-s­ens­itive proteins allow a small amount of calcium to flow into the sarcoplasm but also mechan­ically stimulate the Ryanodine receptors on the SR
•The Ryanodine receptors are the calcium “flood gates” of the SR
–When stimulated by the DHP receptors, the ryanodine receptors allow Ca2+ release from SR into the sarcoplasm
–This increases sarcop­lasmic calcium concen­tration supplying the majority of Ca2+ necessary for contra­ction of skeletal muscle

•For skeletal muscle to contract
–Activ­ation (at neurom­uscular junction)
•Must be nervous system stimul­ation
•Must generate action potential in sarcolemma
–Excit­ati­on-­con­tra­ction coupling
•Action potential propagated along sarcolemma
•Intra­cel­lular Ca2+ levels must rise briefly leading to the onset of contra­ction

•Skeletal muscles stimulated by somatic motor neurons
–Under voluntary contro­l•Axons of motor neurons travel from central nervous system via nerves (bundles of mostly neuron axons) to skeletal muscle
•Each axon may form several branches as it enters whole muscle
•Each axon ending forms a neurom­uscular junction with single muscle fiber

•ACh effects quickly terminated by enzyme acetyl­cho­lin­est­erase in synaptic cleft
–Breaks down ACh to acetate and choline
–Prevents continued muscle fiber contra­ction in absence of additional stimul­ation

•End plate potential (local depola­riz­ation)
–ACh binding opens chemically (ligand) gated ion channels
–Simul­taneous diffusion of Na+ (inward) and K+(out­ward)
•More Na+ diffuses in, so interior of sarcolemma becomes less negative
–Local depola­riz­ation = end plate potential

•Repol­ari­zation – restoring electrical conditions of RMP
–Volta­ge-­gated K+ channels begin to open
–K+efflux (outflow) begins to outpace Na+ influx­•ra­pidly restores resting polarity (makes negative again)
•Na+ are closing, eventually decreasing Na+ influx
–Another muscle fiber depola­riz­ation AP cannot be stimulated
•in refractory period until repola­riz­ation complete
–Event­ually, K+ channels close (lowers K+ efflux)
–Chemical and electrical conditions of resting state restored by Na+-K+pump and K+ leaking out of the cell through K+leak channels

•Nerve impulse (AP) reaches axon terminal volta­ge-­gated calcium channels open ACh released to synaptic cleft
•ACh binds to its receptors on sarcolemma  opens ligand­-gated Na+ and K+ channels  end plate potential 
•Opens voltag­e-gated Na+ channels  AP propag­ation 
•Volta­ge-­sen­sitive proteins in T tubules (DHP receptors) change shape and activate the Ryanodine recept­orsSR releases Ca2+ to cytosol