Neuromuscular Synapse

Resting Membrane Potential and Muscle Contraction

The resting membrane potential results from the distribution of various cations and anions inside and outside of the cell. To initiate muscle contraction, this potential can become depolarized by altering the movement of ions, specifically sodium ions. This process occurs at the neuromuscular junction, the site where a neuron communicates with a muscle cell. The axon terminal of the neuron connects with the muscle cell's membrane across a small space known as the synaptic cleft.

In a neuromuscular synapse, the presynaptic terminal is the neuron side, while the post-synaptic terminal is the muscle cell. In the synaptic cleft, which is filled with extracellular fluid, there is a higher concentration of sodium ions compared to the inside of the cell, where sodium concentration is relatively low. At the nerve ending, synaptic vesicles contain neurotransmitters, specifically acetylcholine, which play a crucial role in muscle contraction. When an action potential reaches the axon terminal, these vesicles release acetylcholine into the synaptic cleft, serving as the signal for muscle contraction.

The binding of acetylcholine to its receptor on the muscle cell membrane opens a specialized channel known as a ligand-gated sodium channel. This channel is initially closed but opens upon acetylcholine’s binding, allowing sodium ions to flow into the muscle cell. The influx of sodium ions occurs from a region of high concentration (the synaptic cleft) to a region of low concentration (the cytoplasm of the muscle cell). This movement of sodium depolarizes the muscle cell, bringing the membrane potential closer to zero, signaling the initiation of muscle contraction.