To generate an action potential, the membrane potential must be stimulated, disturbing the resting balance of charges within the neuron. The first step in this process is the opening of sodium ion channels within the membrane, allowing sodium ions to flow into the cell. This flow occurs due to the concentration gradient where sodium is more concentrated outside the cell than inside, creating a push for sodium ions to enter and making the internal environment of the cell more positive.
The resting membrane potential is generally around -70 to -85 millivolts. This is maintained by the distribution of ions, primarily sodium (Na+) and potassium (K+), across the membrane. The membrane, composed of phospholipids, presents a challenge for ions to cross freely, necessitating specialized channels.
When a stimulus occurs, sodium channels open, resulting in sodium ions flooding into the neuron, which leads to a rapid depolarization of the membrane. The membrane potential can rise from approximately -80 mV to as high as +35 mV during this phase. The rapid influx of sodium ions is crucial as it transforms the electrical state of the membrane, leading to what is termed depolarization.
At around +35 mV, the action potential reaches its peak, leading to the opening of potassium channels. As potassium ions, which are more concentrated inside the cell, start to flow out, they significantly contribute to the repolarization phase. This efflux of K+ helps decrease the overall positive charge inside the neuron and brings the membrane potential back down towards negative values, typically nearing -80 mV again.
Following the repolarization phase, the membrane potential may dip below the resting state, a phenomenon known as hyperpolarization. This can lead to a brief state where the neuron is less likely to generate another action potential until it returns to its resting state.
Depolarization: Sodium ions influx leads to a positive shift in voltage.
Repolarization: Potassium ions efflux restores negative charge inside the neuron.
Hyperpolarization: Membrane potential temporarily falls below resting potential before returning to base.
Calcium ions also play a role, particularly in the neuromuscular junction where they facilitate the release of neurotransmitters. The influx of calcium ions into the presynaptic neuron leads to the exocytosis of neurotransmitters, which are crucial for transmitting signals across the synaptic cleft. These neurotransmitters bind to receptors on the postsynaptic muscle cell, opening sodium channels and initiating muscle action potentials.
The neuromuscular junction serves as a special synapse where motor neurons communicate with muscle fibers. This area includes the axon terminal of the neuron, the motor end plate on the muscle cell, and the synaptic cleft—the gap where neurotransmitter diffusion occurs. The neurotransmitter typically involved is acetylcholine.
Action Potential Arrival: The arrival of an action potential at the axon terminal triggers the opening of voltage-gated calcium channels.
Calcium Influx: Calcium enters the axon terminal, prompting synaptic vesicles containing acetylcholine to fuse with the membrane and release the neurotransmitter into the synaptic cleft.
Binding and Channel Opening: Acetylcholine binds to receptors on the motor end plate, opening sodium channels and leading to depolarization of the muscle cell, thus generating a muscle action potential.
Once an action potential is generated in the muscle cell, it initiates a process called excitation-contraction coupling, which ultimately leads to muscle contraction. The action potential travels along the sarcolemma