Remember that an action potential starts with the diffusion of sodium into the cell. As more sodium enters the cell, more voltage gated sodium channels open up. This leads to depolarization of the cell. With a steady diffusion of sodium into the cell, the threshold stimulus will eventually be attained, and an action potential will be generated. It is the steady diffusion of sodium into the autorhythmic cells which results in an action potential.

An inhibitory post synaptic potential (IPSP) drives the post synaptic cell membrane toward hyperpolarization, and thus away from the threshold necessary to fire an action potential. As a result, the axon requires more stimuli in order to fire an action potential.

It is important to recognize that sodium is flowing into the neuron during depolarization. The area outside of the neuron is electrically positive relative to the area inside of the neuron, resulting in the negative resting membrane potential of the cell. This potential allows positively charged sodium ions to flow from a high concentration of positive charge, towards the negative charge in the cell interior. Because the sodium travels from a region of relatively positive charge to a region of relatively negative charge, it is flowing down its electrical gradient.

Due to action by the sodium-potassium pump, there is also a large concentration of sodium ions outside of the cell, relative to the small sodium ion concentration inside the cell. This imbalance creates a chemical gradient across the axon membrane. The opening of the voltage-gated sodium channels during depolarization allows sodium to flow down chemical gradient from high ion concentration to low ion concentration.

Voltage-gated calcium channels do not cause depolarization in neurons, but are integral to depolarization in muscle. Voltage-gated sodium channels are responsible for neural depolarization; there are no sodium leaky channels in neurons, as these would disrupt the resting potential. Voltage-gated potassium channels actively import potassium, whereas the sodium-potassium pump actively exports potassium. There is no such thing a potassium-calcium pump.

During depolarization, voltage-gated sodium channels open and allow a rapid influx of sodium ions. The membrane voltage rises from its resting potential of -70 mV to 35 mV. Depolarization is not associated with endocytosis of neurotransmitters. 

The answer is saltatory conduction. Saltatory conduction is the term used to define the process of action potential jumping described in the question. The other possbilities, while involved in the nervous system and its function, do not adaquately describe the process in question.

The relative refractory period is the moment directly after an action potential when the neuron can only be stimulated to fire another action potential if there is a larger than normal stimulus. During an action potential, voltage-gated sodium channels open. After the action potential, the channels are gated and cannot be re-stimulated. This period is the absolute refractory period. The secondary gating is released, making the sodium-channels functional again, but the neuron has not been fully restored to resting potential. Release of potassium through voltage-gated potassium channels leads to hyperpolarization until the sodium-potassium pump is able to restore ion balance. This restoration takes longer than the un-gating of sodium channels, creating a period when the cell is hyperpolarized, but the voltage-gated sodium channels are capable of stimulation. If a large enough stimulus overcomes the cell hyperpolarization and reaches threshold, and action potential can still occur. This period is the relative refractory period.

While sodium and potassium maintain important functions in the conduction of action potentials along the axon of the neuron, it is calcium that is responsible for the binding of vesicles containing neurotransmitters to the pre-synaptic membrane. A severe lack of calcium would inhibit the release of neurotransmitters into the synaptic cleft. When the action potential reaches the axon terminal, it stimulates the opening of voltage-gated calcium channels. The resulting influx of calcium binds to synaptic vesicles, initiating the process to release their neurotransmitter contents into the synaptic cleft.

For an action potential to occur, voltage-gated sodium channels must open to cause a sharp depolarization (increase) in the membrane potential. Pairing that information with knowledge that action potentials originate at the axon hillock, no other answer choice makes sense. It is only logical, then, that a high density of voltage-gated channels be present at the location where action potentials are first initiated.

Saltatory conduction is a process that propagates an action potential more quickly down the length of an axon in a "leapfrog" manner. This propagation occurs in the gaps between myelin on an axon, called nodes of Ranvier. Without myelin, these nodes would not exist, and the rate at which an action potential is transmitted would decrease. People suffering with multiple sclerosis (MS) have myelin degradation, and thus have decreased motor and other neurological processes.