Vulnerability and plasticity of monoamine neurotransmitter systems in affective and personality disorders

The monoamine neurotransmitter systems have attracted investigative interest in the last two decades for their putative role in the pathophysiology of two major DSM-III Axis I syndromes: the affective and schizophrenic disorders. The “catecholamine hypothesis” and the “dopamine hypothesis” of schizophrenia were based in part on some of the known pharmacologic effects of the antidepressants, e.g., catecholamine re-uptake antagonism, and the neuroleptics, e.g., dopamine receptor antagonism. Evidence supporting these hypotheses has not always been consistent, but has been sufficient to suggest some disturbances of the monoamine systems are associated with these DSM-III Axis I diagnosis, e.g., abnormalities of noradrenergic metabolite concentrations in the affective disorders and of dopaminergic metabolite concentrations in schizophrenia. More recent data suggests a “serotonergic hypothesis” of impulsivity/aggression, e.g., decreased serotonin metabolites in cerebrospinal fluid (CSF) of aggressive and suicide-attempting patients.