This chapter focuses on the studies of dopamine hypothesis of schizophrenia. The group of disorders known collectively as schizophrenia continues to be a critical problem for modern psychiatry and accounts for large expenditures by society and tragedy for many families. The predominant hypothesis for a neurochemical defect in schizophrenia is the dopamine (DA) hypothesis of schizophrenia, which suggests that there is an excess of DA neuronal activity in specific brain areas in schizophrenic patients. Such excess DA activity could occur through increased presynaptic DA release via increased DA synthesis and/or faulty negative feedback regulation, or through supersensitive postsynaptic DA receptors. The DA hypothesis of schizophrenia is supported by indirect pharmacologic evidence. Drugs such as amphetamine and methylphenidate, which increase central DA function, in high and long-term doses, can produce a paranoid schizophrenic-like syndrome in normal subjects. These drugs also exacerbate positive symptoms, that is, hallucinations, delusions, in schizophrenic patients.

In order to assess the effects of increased CNS serotonergic function in humans on prolactin (PRL), growth hormone (GH), and mood, IV l-tryptophan (TRP) was administered to ten healthy subjects. The TRP infusion induced robust increases in PRL in all ten subjects. A significant increase in GH concentration was also observed, although the response was more variable. The subjects reported feeling significantly more ‘high’, ‘mellow’, and ‘drowsy’ following the TRP infusion in comparison to placebo. These findings indicate an important role for serotonin in PRL and GH secretion, as well as in mood regulation. The IV TRP challenge may be of use in the study of serotonergic function in a variety of neurologic and psychiatric diseases.