EXSS 276 1st Edition Lecture 20 Outline of Last Lecture I. SarcomereII. Pharmacology of NMJIII. The Motor UnitIV. All or None ResponseV. Muscle ToneOutline of Current LectureI. Events in Muscle ContractionII. Excitation-Contraction CouplingIII. Sliding Filament Mechanism of ContractionIV. RelaxationV. SummaryCurrent LectureI. Events in Muscle Contractiona. Arrival of action potential at motor end platei. Nerve impulse travels down axon; arrives at synaptic end bulbsii. Synaptic vesicles release ACh into synaptic clefiii. ACh binds to receptors in motor end plateiv. Ligand-gated channel open; sodium flows into muscle cellv. Sodium flows across sarcolemma making it more positively chargedvi. Change in membrane potential (-55mV) triggers muscle APvii. Muscle AP propagates along sarcolemma and into T tubulesb. Release of calcium from SRi. AP propagation into T tubules causes calcium release channels in SR to openii. Calcium flows out of SR into cytosol around thick and thin filamentsc. Removal of troponin-tropomyosin complexes from binding sitesi. Calcium combines w/ troponin, causing it to change shapeii. Troponin-tropomyosin complex moves away from myosin binding sites onactin filamentsiii. Myosin heads bind to actind. Sliding of actin and myosin filaments to shorten sarcomeresi. ATP hydrolysis (ATP => ADP + P) to energy the myosin headsii. Attachment of myosin and actin to form crossbridgesThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.iii. Power stroke occurs: myosin head rotates towards center of sarcomere toslide thin filament past thick filament toward M-line1. Release ADP and P2. Generates forceiv. Detachment of myosin from actin as myosin head binds to another ATPv. Continues as long as ATP available and calcium near thin filament is sufficiently highvi. Cycle keeps repeating as long as there is:1. ATP available2. Calcium signal3. Physical limitation not reachede. Cessation of action potentiali. AChE breaks down ACh in synaptic cleff. Calcium pumped back into SRi. Calcium release channels in SR closeii. Active transport pumps in SR pump calcium back into SRg. Troponin-tropomyosin complexes cover binding sites i. Calcium around thin filaments decreasesii. Troponin-tropomyosin complexes move back to cover myosin binding sites on actin filaments h. Sarcomeres return to resting length II. Excitation-Contraction Couplinga. Steps connecting muscle excitation w/ contraction (mechanical response)III. Sliding Filament Mechanism of Contractiona. Myosin cross bridges pull on thin filamentsb. Thin filaments slide inwardc. Sarcomeres, muscle fiber and muscle shortend. Notice: thick and thin filaments do not change in lengthIV. Relaxationa. AChE breaks down ACh w/in synaptic clefb. Muscle action potential ceasesc. Calcium release channels of SR closed. Active transport pumps calcium back into SRe. Tropomyosin-troponin complex recovers binding site on actinV. Summarya. Nerve impulse from the brainb. At NMJ-ACh is releasedc. Diffuses across synaptic clef and binds to receptorsd. Ion-gated channels are opene. ACh broken down by AChEf. Threshold was reached, where does AP go?i. Transverse tubules take AP into the cellii. Simulate SRg. Stimulates release of calciumh. Calcium changes shape of troponini. Troponin pulls tropomyosinj. Myosin binds to actin (requires ATP)k. Contraction: power strokes use ATP – pull towards the middle l. How do you stop contraction?i. Calcium pumped back into SR by active transportm. Troponin-tropomyosin complex slides back into position where it blocks myosin binding sites on actinn. Muscle