Muscle voltage-gated calcium channel. A rush of calcium ions

Muscle ContractionMuscle contractions occur every single time a movement is made, whether its running, walking, lifting, sitting, pulling, or even chewing.  They are a result of the tension buildup within the muscle, and energy in the form of a molecule called ATP (adenosine triphosphate) must be in continuous supply. In addition to the requirement of energy, muscles must be somehow stimulated to contract. The neuromuscular junction is the place where motor axons meet axons, transmitting messages from the brain which stimulates the muscle to contract. It all starts with the nerve impulse arriving at the axon terminal of a motor neuron, causing a voltage change of the membrane and the opening of the voltage-gated calcium channel. A rush of calcium ions then enter the axon terminal, causing a shape change to the synaptic vesicles holding the neurotransmitter Acetylcholine (ACh). As a result of the synaptic moving to the membrane of the axon terminal, ACh is liberated by exocytosis into the synaptic cleft. When the ACh moves into the cleft, it binds to the receptor sites of the chemically-gated ion channels on the motor end plate. The channels open which permits an influx of sodium and small efflux of potassium ions(“Actions at Neuromuscular Junction,” n.d. ). This ion exchange causes a local depolarization of the motor end plate and if it passes threshold, an action potential is generated. ACh is released from the receptors and is later broken down by an enzyme called Acetylcholinesterase (AChE) within the cleft. Meanwhile, the action potential propagates along the sarcolemma and down the T-tubules. Then it comes in contact with the sarcoplasmic reticulum, resulting in calcium(“Stages of Neuromuscular Junction,” n.d. ). rushing into the the sarcoplasm of the cell  as the calcium ion channel on the sarcoplasmic reticulum opens.Now that the stimulus has caused the action potential to reach the sarcoplasmic reticulum which stores calcium ions, vital to contraction, the muscle is coming closer to being ready to contract. That leads to the sliding filament theory. It is where thin filaments (actin) and thick filaments (myosin) within the sarcomeres bind to create cross-bridges and slide past one another with the presence of ATP. In the presence of high concentrations of calcium, it diffuses in the sarcoplasm and  binds to troponin in actin. The shape of troponin change and causes tropomyosin to move away from the active site of actin. Now that the binding site on the actin is freed, the myosin head swings back and attaches to actin, forming a cross-bridge connection when ATP is broken down into ADP and P(phosphate group) due to the presence of calcium. The myosin head pivots and bends(aka power stroke) as it pulls the actin inwards sliding it toward the M-line from the release of P(“Sliding Filament,” n.d.). Myosin detaches from the actin and the cross-bridge is broken down when a new  ATP binds itself to myosin head. When ATP is the broken down into ADP and P, the myosin head can again attach to an Actin binding site further along the filament and repeat the process.  This process of muscular contraction can last as long as there’s an adequate ATP and calcium supply. Once the impulse comes to a halt, the tropomyosin covers up the actin, and calcium breaks off from troponin and moves back into the sarcoplasmic reticulum, resulting in the muscle to lengthen and relax.

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