Final answer:
Voltage-gated Ca²⁺ channels are activated by the depolarization of the cell membrane, which is often the result of an action potential. The opening of these channels allows calcium ions to enter the cell, triggering a cascade of events that lead to neurotransmitter release at synapses and muscle contraction at the neuromuscular junction.
Step-by-step explanation:
Voltage-gated Ca²⁺ channels are activated by changes in membrane voltage. When an action potential reaches the axon terminal, it causes depolarization of the membrane. Subsequently, voltage-gated Na⁺ channels open, allowing Na⁺ ions to enter the cell and further depolarize the presynaptic membrane. This increased depolarization triggers the opening of voltage-gated Ca²⁺ channels. The influx of Ca²⁺ ions into the neuron initiates a signaling cascade that promotes the fusion of neurotransmitter-containing synaptic vesicles with the presynaptic membrane and the release of neurotransmitters into the synaptic cleft.
The role of these channels is crucial at synapses, especially at the neuromuscular junction, where the influx of Ca²⁺ ions leads to muscle contraction. These channels also participate in excitation-contraction coupling, as the depolarization of the muscle membrane initiates an action potential that spreads along the membrane. Moreover, in certain types of synapses, the binding of neurotransmitters like glutamate to receptors such as NMDA is necessary for channel activation, but only after depolarization removes an inhibitory Mg²⁺ ion, allowing Ca²⁺ to enter the cell.