The main stages of an action potential are depolarization, hyperpolarization, and repolarization. The resting membrane potential of the cell is roughly –65mV. During depolarization the neuron initiates the action potential by opening voltage-gated sodium channels. This allows an influx of sodium ions, which raises to membrane potential to roughly 50mV. Sodium channels are quick to react to the action potential stimulus, but voltage-gated potassium channels are slower. After the depolarization, the potassium channels open, allowing for a rapid efflux of potassium ions. This causes the membrane potential to rapidly drop, so much so that it becomes more negative than the resting potential. This drop below resting potential is known as hyperpolarization. Repolarization then occurs by action of the sodium-potassium pump, which uses ATP to reestablish the resting potential by removing sodium and importing potassium.

The absolute refractory period occurs when the initial gating mechanism of the sodium channels is activated, making them impervious to stimuli. In contract, the relative refractory period is closely linked to hyperpolarization and describes the period during which the cell can be stimulated, but only if the stimulus is large enough to overcome the hyperpolarized environment and reach threshold.

The action potential is composed of key changes in voltage for the neuronal cell body. The resting voltage in the cell is negative, due to the action of the sodium-potassium pump. When an action potential reaches the cell, voltage-gated sodium channels open, and sodium ions rush into the cell. This raises the voltage inside the cell in a process called depolarization.

As the voltage in the cell rises, the sodium channels begin to close, and voltage-gated potassium channels begin to open. As potassium ions exit the cell, the voltage drops back down to negative once again. This process is called repolarization. It takes a bit longer for the potassium channels to close, which causes a temporary hyperpolarization of the cell; however, once they close and the cell will eventually return to the initial negative resting potential by action of the sodium-potassium pump.

There is a larger number of voltage-gated calcium channels near the synaptic cleft on the pre-synaptic neuron. As an action potential approaches the synaptic cleft, these voltage-gated calcium channels open and allow for a rapid influx of calcium. The sudden influx of calcium ions into the cell causes a release of neurotransmitters into the synaptic cleft.

Sodium and potassium play key roles in establishing the resting membrane potential and propagating the action potential, but do not actually stimulate the release of the neurotransmitter.

Neurotransmitters cross the synaptic cleft to cause a change in the excitability of the downstream neuron. Acetylcholine is an excitatory neurotransmitter matching the description in the question stem. GABA is an inhibitory neurotransmitter and serotonin is responsible for feelings of happiness. Cortisol and epinephrine are hormones, not neurotransmitters, thus they are released into the bloodstream, not the synaptic cleft.

Repolarization is one of the last steps of an action potential, where the cell potential of the neuron is made to be negative in value once again. This step is accomplished by the opening of voltage-gated potassium channels, which allows for potassium to exit the neuron.

Action potentials are unique in that they are a one-way transmission of impulses throughout the nervous system. Action potentials will always be the same amplitude for a given neuron, regardless of the stimulus which caused it; however, the stimulus must be sufficient enough to cross the threshold, or the action potential will not occur. It is because of this feature that action potentials are said to be  "all or nothing" in nature.