Do the Causal Paths to Psychosis Converge on D2High?

Abstract

Despite the many causes of psychosis, most individuals experiencing a psychotic episode improve with antipsychotic drugs. How is it that patients respond to a similar type of drug treatment whether their illness is associated with a major deletion in chromosome 22, or is a result of birth trauma, or a consequence of the family’s genetic predisposition for psychosis, or an end product of the use of street drugs? Why would so many different pathophysiological routes be blocked when blocking dopamine receptors? A related question is why schizophrenia patients are supersensitive to dopamine-like stimulants (1). Is this related to the relapse seen when switching from a traditional antipsychotic to a medication such as aripiprazole (2, 3)? These clinical questions are addressed by looking to animal models of psychosis, as limited as these models may be for schizophrenia itself (4). There are many animal models of human psychosis. They include strategically placed brain Do the Causal Paths to Psychosis Converge on D2High?