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Now for more details on the major players, as seen on the previous page:

Receptors (proteins that are stuck to the wall of the receiving neuron) act as receivers for neurotransmitters. When a neurotransmitter is sent from one neuron to the next, the intention is for it to hit a receptor and transmit (well, help transmit!) the signal over.

Ion channels act very quickly to balance and start/stop the conduction of an impulse down an individual neuron. Many are "voltage-gated", meaning that they react quickly to a change in a neuron (the battery)'s voltage. Some ion channels are actually activated by neurotransmitters, meaning that when hit by a neurotransmitter, the ion channel will function and cause a relatively rapid electrical reaction.
It is possible that changing how an ion channel works (via, say, meds) can change the way messages are sent through the synapse. In particular, most of the anticonvulsant (anti-epilepsy and anti-bipolar disorder) medications are thought to work by hitting ion channels.

Another major player in this stuff is the "reuptake pump" (also known as "transporter" or "transport pump"). Located on the presynaptic ('before the synapse') neuron, the function of these proteins is preventing the synapse from having too much of X neurotransmitter. If there's too much neurotransmitter, the signal sent may be too strong and therefore undesirable. So, we've got reuptake pumps to help our neurons and synapses function normally. These pumps function by using the voltage across the neuron (i.e., as if they were battery-powered).
Arguably, reuptake pumps are the most targeted devices when it comes to neurological and psychiatric medications. PROZAC and its relatives work by blocking the serotonin (5-HT) reuptake pump, a protein known as SERT. Intuitively, this encourages the synapse to flood with serotonin --- more on that later.
Vesicles are nothing but little pockets within the cell specifically, ones that contain neurotransmitter molecules. They are responsible for moving neurotransmitters from the interior of the presynaptic neuron into the synapse such that the message is sent. Drugs that function as releasing agents promote yanking neurotransmitters out the vesicles and into the synapse (for better or worse).
Another player in our neurochemical balance is the "degradation" enzyme (that one wasn't diagrammed on the previous page).
Enzymes in general are large bodily proteins that make chemical reactions happen. Think of them as little molecular nanobots that peform chemical reactions.
In this case, degradation enzymes specifically inactivate neurotransmitter molecules, turning them into a useless form. Much like the reuptake pump, this action reduces the overall neurotransmission and brings it back to "balance" if the transmission is too high. Now, please note that degradation enzymes are located not in the synapse, but inside individual neurons. MAOIs (a class of drugs that includes antidepressants and anti-parkinson syndrome agents) as well as Acetylcholinesterase inhibitors (anti-dementia drugs) act upon degredation enzymes. Again, more on that later.