Final answer:
After depolarization, voltage-gated sodium and calcium channels open, leading to neurotransmitter release into the synaptic cleft. The membrane then repolarizes, and neurotransmitters are degraded or reabsorbed, restoring the synapse for the next action potential.
Step-by-step explanation:
After a microelectrode delivers a current pulse that depolarizes the presynaptic terminal above threshold, several key events unfold at the molecular level. Initially, the depolarization opens voltage-gated sodium channels, allowing sodium ions (Na+) to rush into the neuron, further depolarizing the presynaptic membrane. This causes a chain reaction leading to the opening of voltage-gated calcium channels, facilitating an influx of calcium ions (Ca2+) into the cell. The increased Ca2+ concentration inside the presynaptic terminal triggers a cascade that results in the fusion of synaptic vesicles with the presynaptic membrane. These vesicles contain neurotransmitters, which are then released into the synaptic cleft.
The released neurotransmitters bind to receptors on the postsynaptic neuron, initiating a response in the receiving cell. After the action potential, the membrane repolarizes as potassium channels open, allowing potassium ions (K+) to exit the neuron, returning the membrane potential to a negative value, and entering the refractory period. Eventually, sodium-potassium pumps help restore the resting membrane potential of approximately -70 mV.
Meanwhile, neurotransmitters in the synaptic cleft are either degraded by enzymes such as acetylcholinesterase (AChE) in the case of acetylcholine or are reabsorbed by the presynaptic cell, allowing the postsynaptic neuron to recover and be ready for the next synaptic signal.