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Full curriculum

Full curriculum
  1. Ligand-gated ion channels as fast cell-surface receptors
  2. Calcium-triggered synaptic vesicle release
  3. Neurotransmitter clearance and termination of chemical synaptic signals
  4. Neuromuscular junction and motor end-plate excitation
  5. Calcium control of skeletal-muscle contraction through troponin and tropomyosin
  6. Skeletal-muscle excitation–contraction coupling through T-tubules and sarcoplasmic reticulum
  7. Skeletal-muscle relaxation by calcium reuptake into the sarcoplasmic reticulum

Unit content

Neuromuscular junction and motor end-plate excitation

A neuromuscular junction (NMJ) is the specialized chemical synapse between a somatic motor neuron, a neuron that directly controls skeletal muscle, and a skeletal muscle fiber, an elongated skeletal-muscle cell.

The presynaptic motor-neuron terminal contains vesicles filled with acetylcholine (ACh). The postsynaptic region of the muscle membrane is called the motor end plate and contains a high density of nicotinic acetylcholine receptors, ligand-gated cation channels.

From motor-neuron spike to muscle depolarization

When a motor-neuron action potential reaches the terminal:

  1. presynaptic voltage-gated Ca$^{2+}$ channels open;
  2. Ca$^{2+}$ entry triggers synaptic-vesicle exocytosis;
  3. ACh diffuses across the synaptic cleft;
  4. ACh binds nicotinic receptors on the motor end plate;
  5. receptor channels open and generate a local graded depolarization called the end-plate potential.

The receptor channel conducts several cations. Under normal skeletal-muscle ionic conditions, the net effect near resting voltage is inward positive current and depolarization.

The end-plate potential is graded; the muscle action potential is regenerative

The end-plate potential varies with synaptic activation and remains local rather than regenerating itself across the fiber. If it depolarizes nearby muscle membrane sufficiently, voltage-gated Na$^+$ channels open and initiate a muscle-fiber action potential.

motor-neuron action potential
        ↓
ACh release
        ↓
end-plate potential
        ↓
voltage-gated Na+ channels
        ↓
muscle action potential

Thus ACh receptors do not themselves propagate the action potential over the whole fiber; they provide the local depolarization that triggers regenerative voltage-gated excitation.

Transmission must terminate

Acetylcholinesterase rapidly hydrolyzes ACh in the synaptic cleft. Removal of ACh allows nicotinic receptors to close and prevents one presynaptic signal from producing indefinite muscle excitation.

The NMJ therefore specializes general chemical-synapse machinery to convert a motor-neuron action potential into a muscle-fiber action potential with high reliability.