Final answer:
Neurotransmitters control the initiation or inhibition of action potentials in postsynaptic neurons by binding to receptors and causing hyperpolarization or depolarization, respectively, of the postsynaptic membrane. Inhibitory neurotransmitters cause a hyperpolarizing IPSP, and excitatory neurotransmitters cause a depolarizing EPSP, thus influencing the likelihood of an action potential firing. These neurotransmitters act during synaptic transmission, facilitated by voltage-gated calcium channels in the presynaptic neuron.
Step-by-step explanation:
Neurotransmitters play a crucial role in the modulation of an action potential during neural communication. They are released from the synaptic vesicles of the presynaptic neuron into the synaptic cleft, where they bind to specific receptors on the postsynaptic neuron.
Depending upon the type of neurotransmitter, this binding can cause either an excitatory or inhibitory effect on the postsynaptic neuron.
Inhibitory neurotransmitters, such as GABA (gamma-aminobutyric acid), cause hyperpolarization of the postsynaptic membrane by opening Cl- ion channels. This hyperpolarization leads to an Inhibitory Postsynaptic Potential (IPSP), which makes the neuron less likely to fire an action potential by increasing the negative charge inside the cell, thereby moving the membrane potential further from the threshold needed to trigger an action potential.
On the other hand, excitatory neurotransmitters like acetylcholine, when released into the synapse, result in the opening of Na+ channels and cause a depolarizing Excitatory Postsynaptic Potential (EPSP), making the neuron more likely to fire an action potential by moving the membrane potential closer to the threshold.
Neurotransmitters act during the synaptic transmission stage of an action potential when the signal is being passed from one neuron to the next. Voltage-gated calcium channels in the presynaptic neuron play an essential role in this process as they trigger the release of neurotransmitters into the synaptic cleft in response to an arriving action potential.
The subsequent binding of these neurotransmitters to their respective postsynaptic receptors converts the chemical signal back to an electrical signal, completing the communication between neurons.