The earliest and probably most widely accepted scientific theory of<unk>  action is the monoamine hypothesis (which can be traced back to the 1950s), which states that depression is due to an imbalance (most often a deficiency) of the monoamine neurotransmitters (namely serotonin, norepinephrine and dopamine). It was originally proposed based on the observation that certain hydrazine anti-tuberculosis agents produce<unk>  effects, which was later linked to their inhibitory effects on monoamine oxidase, the enzyme that catalyses the breakdown of the monoamine neurotransmitters. All currently marketed<unk> s have the monoamine hypothesis as their theoretical basis, with the possible exception of agomelatine which acts on a dual melatonergic-serotonergic pathway. Despite the success of the monoamine hypothesis it has a number of limitations: for one, all monoaminergic<unk> s have a delayed onset of action of at least a week; and secondly, there are a sizeable portion (>40%) of depressed patients that do not<unk> equately respond to monoaminergic<unk> s. A number of alternative hypotheses have been proposed, including the glutamate, neurogenic, epigenetic, cortisol hypersecretion and inflammatory hypotheses.
Antidepressant
Antipsychotic
Appetite stimulant
Mood stabilizer
Tetracyclic antidepressant
Tricyclic antidepressant
Atypical antidepressant
Antimanic drugs