In a neuron, the movement of Na+ and K+ across the membrane occurs at specialized parts of the axon called Nodes of Ranvier—gaps between the protective glial cells that insulate the passage of signals. The movement of these ions gives rise to what is called an action potential: the event in a neural axon that relays a message further down from the soma and the dendrites to the terminus of the neuron. Typically, the concentration of sodium ion inside of a cell is less than that outside of it. Voltage-gated ion channels gradually allow more and more sodium into the cell body of the axon of a neuron, and once the influx of sodium depolarizes the cell (makes the positive charge of the inside of the membrane similar to that of the outside, usually about -55mV) to a significant degree, the cell exceeds its threshold potential and opens all of the sodium and potassium ion channels. The surge of ions into the cell pushes upward to the next Node of Ranvier, propagating the action potential until it eventually reaches the axon terminal at the other end.
The release of neurotransmitters into the synaptic cleft occurs via a different biochemical process. When action potentials reach the end of the axon, they trigger voltage-gated calcium (Ca2+) channels to open, leading to a rush of Ca into the presynaptic terminal. This Ca binds to special receptors in the terminal that leads to the formation of synaptic vesicles. These vesicles absorb a particular neurotransmitter—Acetylcholine, dopamine, and others—and then fuse with the cell membrane facing the synaptic cleft. The vesicles can fuse with the presynaptic membrane because their own cell membranes consist of the same molecules as that of the cell. Once the vesicle fuses with the membrane, the outer barrier opens and the neurotransmitter can spill into the synaptic cleft to bind with cell-surface receptors on the post-synaptic membrane.