The way neurochemistry is treated in the popular press, you’d think the presence of a neurotransmitter in the brain had a clear effect on consciousness. Increase the level of chemical X in the brain, you get happy, decrease the level of the same, you get sad. And so journalists have got into the habit of labeling neuromolecules (at least the best researched of them) in simplistic ways: oxytocin is the “cuddle hormone,” dopamine is the “reward neurotransmitter,” serotonin is the “depression neurotransmitter” (or the “antidepression neurotransmitter”; I don’t think the press is too clear on that one).
In the actual brain, however, it doesn’t work that way. It is true that certain neurotransmitters are associated in the scientific literature with certain kinds of behaviors or the onset of certain moods. But the same neurotransmitter which excites a neural circuit in one part of the brain can be useful for inhibiting a signal in another circuit in another part of the brain.
The reason this is possible is due to the many different variety of receptor sites which accept any given neurotransmitter. Eleven different kinds of receptor sites, for example, have been identified which are activated by Serotonin. (See this table at Wikipedia for a breakdown of the different Serotonin receptors and what neurological events they govern.)
There are other reasons not to focus too heavily on individual neurotransmitters. For a number of decades, the leading neurological model of schizophrenia stated that it came about as a result of extraordinarily high levels of dopamine in the brain. Drugs were developed to either reduce the amounts endogenously produced or to block dopaminergic receptor sites, resulting in a lessoning of schizophrenic symptoms but also Parkinsonism and catatonia. A more contemporary view of schizophrenia suggests that it is the result of an imbalanced distribution of dopamine in the brain, too much in one area and not enough in another.
