When you clicked your mouse button to get to this page, a remarkable series of events took place. You thought (consciously or subconsciously) about moving your finger. A signal went from your higher brain regions to your spinal cord. A selected group of motor neurons in your spinal cord were activated. The activated motor neurons instructed a specific group of skeletal (voluntary) muscles to contract, and voilà you clicked the mouse button.
Every one of the voluntary (skeletal or striated) muscles in your body is controlled by signals generated in the motor neurons of your spinal cord or brain stem. When you need to move something by muscular activity a neurochemical signal crosses from motor nerve to skeletal muscle at the structure known as the neuromuscular junction (NMJ). And for every single vertebrate organism, the system of communication is essentially identical. Why mess with success?
Like all nerve cells, the motor neuron has a large central region known as the cell body or soma, in which resides the nucleus (with the cell’s DNA) and a large percentage of all the biosynthetic machinery the cell needs to survive. Unlike non-nerve cells, all neurons also have thin projections of their cell membrane that stretch away from their soma. These projections are known as either axons or dendrites. The axon of a nerve cell is the single projection that allows a nerve cell to communicate with the target cell it hopes to modulate. The dendrites and the soma receive incoming signals from other nerves. All of these signals occur at what are referred to as synapses.
When told to stimulate a skeletal muscle, the motor neuron activates its own signal, a property shared by all nerve cells, by generating what is known as an “action potential”. By allowing specific ions to now flow across the cell membrane (such as sodium ions), a change in the electrical properties of the cell occurs. This signal is propagated in just this manner all the way to the end of the axon where it causes the release of the critical signaling molecules, neurotransmitters. For every vertebrate species the neurotransmitter used by motor neurons is the compound known as acetylcholine.
When the motor neuron releases acetylcholine at the NMJ, it diffuses across the very narrow ‘synaptic cleft’ and binds to acetylcholine receptors in the muscle cell membrane. Muscle has an extraordinarily high concentration of these receptors directly across from the end of the motor axon. The acetylcholine receptors open an ion channel in response to binding of acetylcholine and the muscle initiates its own action potential.
When stimulated by acetylcholine from the motor neuron and subsequently starting an action potential, electrical changes in the muscle cause the release of calcium ions inside the muscle. This release leads to a change in the biochemical behavior of molecules inside the muscle which leads to the sliding of the thick and thin filament proteins along each other inside the muscle cell. These sliding filaments lead to contraction of the cell and the ability to generate force so the mouse button can be clicked. At the end of the cycle, enzymes within the synaptic cleft degrade some of the acetylcholine molecules and the motor nerve terminal takes up the remainder.
Numerous toxins can alter the communication between motor nerve and skeletal muscle. One such molecule, botulinum toxin, blocks the capacity of motor nerves to release acetylcholine, which stops muscle contraction. Not such a good thing if you have fallen victim to botulism poisoning, but good for appearances if you have had an injection of Botox into facial muscles for cosmetic reasons.