Proper functioning of the synaptic connections between nerve cells and muscle fibers, known as neuromuscular junctions, is essential to life. The digital image featured in this section is a confocal micrograph of mouse neuromuscular junctions in which the acetylcholine receptors at the motor endplates are labeled red with alpha-bungarotoxin. In addition, the protein synaptophysin, which is a component of the transmitter-rich synaptic vesicles, is labeled green, while the innervating axons are labeled blue.

Mouse Neuromuscular Junctions Specimen: Fluorescent triple label Technique: Confocal Microscopy

Neuromuscular junctions consist of nerve fibers divided into numerous branches, each ending on a region of muscle fiber referred to as the end-plate. Thousands of receptors are embedded in a single end-plate, forming ion channels through the cell membranes. Stimulation by a nerve impulse causes the branches to release small amounts of the chemical acetylcholine from synaptic vesicles. The acetylcholine then stimulates a protein on the muscle fiber surface, the acetylcholine receptor, triggering a series of reactions within the muscle and causing it to contract. In order to prevent extended muscle response to a single nerve signal, the acetylcholine is then broken down by the enzyme cholinesterase.

Various diseases, such as myasthenia gravis and the less common Lambert-Eaton syndrome, are characterized by a malfunctioning of impulse transmissions at neuromuscular junctions. The autoimmune maladies cause weakness and fatigue and can be life threatening when they interfere with respiration. Myasthenia gravis occurs when the body’s antibodies attack the muscles' acetylcholine receptors, disrupting nerve-muscle communication, while Lambert-Eaton syndrome develops when nerve cells are unable to release normal amounts of acetylcholine.