The Synapse functions in the following manner:

      Once the axon has reached its threshold of excitation, an action potential will be propogated at a rate that is proportional to the diameter of the axon, and that is further accelerated by the presence of the Glial Myelin Sheaths, which restrict the active conducting points to the Node of Ranvier.
     Nodes of Ranvier, are the only sites on the myelinated axons at which the axonal membrane is directly exposed to the extracellular fluid, and hence are the only sites at which transmembrane ionic flows can take place.   Therefore, instead of the action potential propogating from minutely contiguous sites of the membrane, the action potential in the myelinated axon leaps from node to node.

      When an action potential reaches the terminal of the presynaptic neuron, some of its synaptic vesicles release their neurotransmitter chemical into the Synaptic Cleft.    This neurotransmitter binds weakly to the receptors found on the postsynaptic cell membrane, after which it is either quickly washed away by the extracellular fluid produced by Glial cells and then neutralized, or it is taken back into the presynaptic neuronal terminal via its membrane for reuse.

      Receptors  (specialized protein molecules on the surface of the postsynaptic or target cell, or within the nucleus of the target cell's cytosol), have binding sites with a high affinity for a particular signaling substance (a hormone, pheromone, Poly-Peptide, or in this case a Neurotransmitter)!   Here, we may refer to the signaling substance as the ligand (a substance that binds to or fits a site).   When the signaling substance binds to the receptor, the receptor-ligand complex initiates a sequence of reactions that changes the activity of the cell.

      Ligand binding induces a conformational change in the receptor that opens a specific ion channel in the protein itself.   The resultant flow of ions changes the electric potential across the cell membrane, leading to the depolarization and consequently the production of an action potential, in the postsynaptic cell.

      Poly-Peptide  secreting neurons differ in biology from those neurons using amino acids and monoamines in ways other than the molecular structure of their transmitters.   The amino-acid or monoamine transmitters are formed from dietary sources by one or two intracellular enzymatic steps;  the end product of these enzymatic actions is the active transmitter molecule which is then stored in the nerve terminal until release.   After release, the transmitter (or choline in the case of ACh) can be re-accumulated back into the nerve terminal by the energy-dependent active re-uptake property, thus conserving the requirement for de novo synthesis.
      Peptide-secreting cells employ a much more formidable approach:   Synthesis is directed by messengerRNA on ribosomes and thus this synthesis can only take place in the Perikaryon on dentrites of a neuron.   Further, all peptides are synthesized as part of a much larger precursor molecule (or Prohormone) which has no biological activity and from which the active peptide is cleaved by special processing peptidases.   The process for peptides thus starts with ribosomal synthesis of the prohormone, which is then packaged int vesicles in the smooth endoplasmic reticulum, and transported from the perikaryon to the nerve terminals for eventual release.