Biology – Control and coordination in mammals | e-Consult

Muscle contraction is a complex process involving the coordinated action of the neuromuscular junction, the T-tubule system, and the sarcoplasmic reticulum (SR). Here's a breakdown of their individual and combined roles:

1. Neuromuscular Junction (NMJ): This is the synapse between a motor neuron and a muscle fibre. When an action potential arrives at the motor neuron's axon terminal, it triggers the influx of calcium ions (Ca²⁺) into the terminal. This influx causes vesicles containing acetylcholine (ACh) to fuse with the presynaptic membrane and release ACh into the synaptic cleft.
2. Acetylcholine Binding and Muscle Fibre Activation: ACh diffuses across the synaptic cleft and binds to acetylcholine receptors (AChRs) on the muscle fibre's sarcolemma (plasma membrane). This binding depolarizes the sarcolemma, generating an end-plate potential (EPP). If the EPP reaches threshold, it triggers an action potential in the muscle fibre.
3. T-Tubule System: The sarcolemma is closely associated with the T-tubule system, which are invaginations of the sarcolemma that penetrate deep into the muscle fibre. These T-tubules are continuous with the sarcolemma and allow the action potential to rapidly propagate throughout the muscle fibre. The action potential travels along the sarcolemma and down the T-tubules.
4. Sarcoplasmic Reticulum (SR): The T-tubules are in direct contact with the SR, a network of tubules that stores calcium ions (Ca²⁺). The action potential travelling down the T-tubules stimulates the SR to release Ca²⁺ into the sarcoplasm (cytoplasm of the muscle fibre). This release is mediated by voltage-sensitive calcium channels (dihydropyridine receptors) that are part of the SR membrane.
5. Calcium and Myosin Binding: The increase in cytoplasmic Ca²⁺ binds to troponin, a protein complex on the thin filaments (actin). This binding causes a conformational change in tropomyosin, which in turn exposes the myosin-binding sites on actin. This allows myosin heads to bind to actin, forming cross-bridges.
6. Muscle Contraction: The binding of myosin to actin initiates the power stroke, which pulls the thin filaments towards the center of the sarcomere, causing muscle fibre shortening and contraction. This process requires ATP for both the initial binding of myosin to actin and for the subsequent detachment of myosin heads after the power stroke.
7. Calcium Reuptake: After the action potential has passed, Ca²⁺ is actively transported back into the SR by Ca²⁺ pumps (SERCA). This reduces the cytoplasmic Ca²⁺ concentration, allowing the troponin-tropomyosin complex to block the myosin-binding sites on actin, and the muscle fibre relaxes.