Ace the 2025 ABPN Challenge – Rock Your Path to Psychiatry Success!

The release of neurotransmitters at synaptic terminals is critically dependent on calcium ions (Ca2+). During an action potential, when a neuron depolarizes, voltage-gated calcium channels in the presynaptic membrane open in response to the change in membrane potential. This influx of calcium ions into the cell plays a fundamental role in neurotransmitter release.

When calcium enters the presynaptic terminal, it triggers a cascade of events that leads to the fusion of synaptic vesicles with the membrane and the release of neurotransmitters into the synaptic cleft. This process is known as exocytosis and is essential for neuronal communication.

Furthermore, calcium ions are also involved in various signaling pathways that activate other ion channels, thus contributing to the excitability and signaling properties of neurons. They play a role in muscle contraction, gene expression, and synaptic plasticity, showing their broad significance in both physiological and pathophysiological contexts.

In contrast, sodium (Na+) is primarily responsible for the initial depolarization phase of the action potential, potassium (K+) mainly facilitates repolarization, and chloride (Cl−) often inhibits action potentials, hence not directly participating in neurotransmitter release. Therefore, calcium's unique role in neurotransmitter release