s are responsible for regulation of serotonin
levels throughout the brain
. Their function is neuromodulator
y; that is, they aren't specifically involved in processing of thought
, instead they regulate the overall function of those neurons
which are. Cell bodies
of these neurons are located in the raphe nucleus
, which is part of the medulla
s project from there into all areas of the cerebral cortex
and limbic system
, as well as descending down the spinal cord
. I couldn't find any specific numbers for human
s, but in the rat brain serotonin
neurons account for around 160,000 out of the twenty billion
total neurons, and human percentages shouldn't be terrifically different.
Since there are so few serotonin neurons to go around, their axons tend to be very long (a foot or more) and each axon projects to many places throughout the brain. When exposed to fenfluramine or ecstasy (MDMA, MDA, MDEA, and so forth), it is the axons which release the serotonin that give these drugs their effect. Likewise, it is the axon that is destroyed when it takes up dopamine after use of these drugs. Contrary to popular belief the neuron itself is very rarely killed, and it can thus continue to branch out new axon terminals throughout the brain, restoring function lost to brain damage. However, it's not known if the axons will regrow to all of the areas in which they were killed off, so it's probably wisest not to do the damage in the first place.
The primary way serotonin leaves the synapse is by reuptake by the serotonin neuron. After firing, serotonin neurons monitor the amount of serotonin left in the synapse and reuptake enough to put the level within normal bounds. When serotonin is artificially agonized (ie, with the drugs mentioned above), the reuptake process is constantly being forced on. Serotonin reuptake transporter proteins aren't terribly specific, they'll uptake all kinds of things besides serotonin: dopamine, LSD, prozac, whatever. Normally this isn't a problem, as reuptake is triggered by the after-effects of firing, but when forced to reuptake constantly, the transporters grab anything, including chemicals which are toxic to the neuron. Thus, ecstasy doesn't kill the axons itself; rather, the axons take up dopamine which they can't process, and it's the dopamine concentration which ends up being toxic.
Serotonin synthesis happens within these neurons, from tryptophan to 5-hydroxytryptophan (both of which can cross the blood-brain barrier) then to serotonin (which cannot). Increasing the amount of 5-hydroxytryptophan in the bloodstream will increase the amount available to the serotonin neurons, so more serotonin can be synthesized. This is the action behind the antidepressent properties of 5-HTP -- it increases synaptic serotonin as much as an SSRI would, but in a less invasive way.