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Muscle contraction. Students participating in the presentation: 1- naif aljabri 430101612 2- yousif alessa 430105885 3- faris abalkheel 430101692 4- Ali Moshaba AL-Ahmary 430103532 5-abdulelah bin numay 430104473. Skeletal muscle. Skeletal muscle. Skeletal muscle.
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Muscle contraction
Students participating in the presentation: 1- naif aljabri 430101612 2- yousif alessa 430105885 3- faris abalkheel 430101692 4- Ali Moshaba AL-Ahmary 430103532 5-abdulelah bin numay 430104473
Skeletal muscle&Muscle filaments • Skeletal muscle • Contraction of skeletal muscle is under voluntary control. • each skeletal muscle cell is innervated by a branch of a motoneurons . • Muscle filaments • each muscle fiber behaves as a single unit • is multinucleate and contains myofibrils • the myofibrils are surround by sarcoplasmic reticulum are invaginated by transverse tubules ( t tubules) • each myofibril contains interdigitating thich and thin filaments.
Thich filaments&Thin filaments • Thich filaments • are comprised of a large molecular weight protein called myosin • Thin filaments • are composed of 3 proteins: 1- actin.2-tropomyosin.3-troponin.
CYTOSKELTAL PROTEINS
Transverse tubule and the sarcoplasmic reticulum • Transverse tubule and the sarcoplasmic reticulum • are continuous with the sarcolemmal membrane and invaginated deep into the muscle fiber, making contact with terminalcisternae of the sarcoplsmic reticulum.
Excitation-contraction coupling Excitation-contraction coupling • In skeletal muscle the method of excitation contraction coupling relies on the ryanodine receptor being activated by a domain spanning the space between the T tubules and the sarcoplasmic reticulum to produce the calcium transient responsible for allowing contraction. • The motor neuron produces an action potential that propagates down its axon to the neuromuscular junction. • The action potential is sensed by a voltage-dependent calcium channel which causes an influx of Ca2+ ions which causes exocytosis of synaptic vesicles containing acetylcholine. • Acetylcholine diffuses across the synapse and binds to nicotinic acetylcholine receptors on the myocyte, which causes an influx of Na+ and an efflux of K+ and generation of an end-plate potential.
Excitation-contraction coupling • The end-plate potential propagates throughout the myocyte's sarcolemma and into the T-tubule system. • The T-tubule contains dihydropyridine receptors which are voltage-dependent calcium channels and are activated by the action potential. • Opening of the Ryanodine receptors causes and flow of Ca2+ from the sarcoplasmic reticulum into the cytoplasm. • Ca2+ released from the sarcoplasmic reticulum binds to Troponin C on actin filaments, which subsequently leads to the troponin complex being physically moved aside to uncover cross-bridge binding sites on the actin filament.
Excitation-contraction coupling • By hydrolyzing ATP, myosin forms a cross bridges with the actin filaments, and pulls the actin toward the center of the sarcomere resulting in contraction of the sarcomere. • Simultaneously, the sarco/endoplasmic reticulum Ca2+-ATPase actively pumps Ca2+ back into the sarcoplasmic reticulum where Ca2+ rebinds to calsequestrin. • With Ca2+ no longer bound to troponin C, the troponin complex slips back to its blocking position over the binding sites on actin. • Since cross-bridge cycling is ceasing then the load on the muscle causes the inactive sarcomeres to lengthen.
Mechanism of tetanus Mechanism of tetanus • A single action potential result in the release of a fixed amount of ca+ from the sarcoplasmic reticulum which produce a single twist is terminated ( relaxation occurs ) when the sarcoplasmic • Step 1: At the end of the previous round of movement and the start of the next cycle, the myosin head lacks a bound ATP and it is attached to the actin filament in a very short-lived conformation known as the 'rigor conformation'. • Step 2: ATP-binding to the myosin head domain induces a small conformational shift in the actin-binding site that reduces its affinity for actin and causes the myosin head to release the actin filament.
Mechanism of tetanus • Step 3: ATP-binding also causes a large conformational shift in the 'lever arm' of myosin that 'cocks' the head into a position further along the filament. ATP is then hydrolysed, but the inorganic phosphate and ADP remain bound to myosin. • Step 4: The myosin head makes weak contact with the actin filament and a slight conformational change occurs on myosin that promotes the release of inorganic phosphate. • Step 5: The release of inorganic phosphate reinforces the binding interaction between myosin and actin and subsequently triggers the 'power stroke'. The power stroke is the key force-generating step used by myosin motor proteins; forces are generated on the actin filament as the myosin protein reverts back to its original conformation. • Step 6: As myosin regains its original conformation, the ADP is released, but the myosin head remains tightly bound to the filament at a new position from where it started, thereby bringing the cycle back to the beginning.
