(USMLE topics) The neuron-muscle relationship and generation of action potential in skeletal muscle cell.

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A skeletal muscle contracts only when stimulated by nerve impulses from a motor neuron.
The axon of a motor neuron usually gives out many branches, supplying multiple muscle fibers. These fibers constitute a motor unit. Small motor units are found in muscles that require finer control, for example, muscles that are responsible for subtle movements of the eyes. Large motor units are found in larger muscles that require strength, such as muscles of the arms and legs.
The strength of a muscle contraction is determined by the number of motor units that are activated at one time. Even at rest, most muscles are in a partial contraction state, called muscle tonus, which is maintained by alternating activation of a small number of motor units.
The connection between a motor neuron and a muscle fiber is called a neuromuscular junction, which is basically a chemical synapse between the nerve terminal and a specialized area of muscle cell membrane called the motor end-plate. When an action potential reaches the nerve terminal, it causes the release of the neurotransmitter acetylcholine into the synaptic space. Acetylcholine then binds to nicotinic receptors on the end-plate. Nicotinic receptors are ligand-gated ion channels. Upon binding to acetylcholine, they open to allow sodium to enter the cells, depolarizing the cell membrane, producing the so-called end-plate potential.
An action potential is generated in the muscle cell only when the end-plate potential reaches the threshold required to activate voltage-gated sodium channels located outside the end-plate, in the neighboring membrane. When activated, these channels allow faster influx of sodium, further depolarizing and eventually reversing the polarity of the cell membrane. At this point, voltage-gated potassium channels open for potassium to move out, quickly returning membrane voltage to its original resting value.
Once generated, the action potential spreads like a wave thanks to similar voltage-gated ion channels located throughout the muscle fiber. The action potential also runs deep into the fiber via T-tubules, to reach the sarcoplasmic reticulum. Here, it activates voltage-gated calcium channels, releasing calcium from the sarcoplasmic reticulum into the cytosol of muscle cells. Calcium then sets off muscle contraction by the “sliding filament mechanism”. This mechanism is described in another video.
Another important component of the neuromuscular junction is the enzyme acetylcholinesterase. This enzyme removes all acetylcholine molecules that do not immediately bind with a receptor and those that are done activating a receptor. The enzyme action essentially terminates synaptic activation, giving the muscle time to relax, and thus preventing continuous contraction that would result in muscle spasms.
Substances that cause muscle weakness or paralysis do so by interfering with the function of neuromuscular junction:
- Botulinum toxin prevents acetylcholine release from the presynaptic side of the junction.
- Some other toxins attach to nicotinic receptor, blocking acetylcholine from binding, but do not open the ion channel.
- Certain drugs lodge into the channel of nicotinic receptor, blocking the passage of sodium.
All these substances prevent activation of muscle cells and cause flaccid paralysis.
On the other hand, some pesticides inhibit acetylcholinesterase, preventing degradation of acetylcholine, causing continuous activation of muscles. That’s how they induce muscle spasms and cause spastic paralysis.

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