Depolarization of the Triad

Neuromuscular Synapse and Muscle Cell Depolarization

At the neuromuscular synapse, a crucial signaling event occurs, leading to the depolarization of the muscle cell near the neuromuscular junction. This process begins when the innervating neuron releases acetylcholine, which opens ligand-gated channels in the postsynaptic membrane. As a result, sodium influx occurs from the synaptic cleft into the sarcoplasm of the muscle cell, leading to a localized depolarization of the muscle membrane, known as the sarcolemma.

The depolarization then spreads along the sarcolemma and into the transverse tubules, facilitated by voltage-gated sodium channels. While the extracellular space around the synaptic cleft and transverse tubules contains high concentrations of sodium, the cytoplasmic compartment of the muscle cell has comparatively lower sodium levels. This influx of sodium progressively propagates along the sarcolemma and transverse tubules. Subsequently, it triggers the opening of voltage-gated calcium channels located in the terminal cisternae of the sarcoplasmic reticulum, which contains a high concentration of calcium.

As sodium continues to enter the muscle cell, calcium is released from the sarcoplasmic reticulum into the surrounding sarcoplasm. This release of calcium ions is significant as it ultimately initiates muscle contraction. The relationship between sodium movement into the muscle cell and calcium release from the sarcoplasmic reticulum serves as the mechanism by which the depolarization at the neuromuscular junction leads to the activation of myofibrils and muscle contraction, illustrating the critical interplay of ionic concentrations for muscle function.