[Truncated abstract] The dopamine theory of schizophrenia remains the dominant model for the neural correlates of positive psychotic symptoms in schizophrenia. The evidence for this model has been accumulating for over 50 years and includes: all antipsychotic medications are dopamine D2 receptor antagonists or partial agonists, direct or indirect dopaminergic agonists can induce symptoms of psychosis in psychosis-naïve populations, psychosis is precipitated by lower doses of stimulants in people with schizophrenia, and there are a number of neurophysiological alterations in the dopamine system of people with schizophrenia. Amphetamine has been one of the central compounds for investigating the latter three points, and therefore its effects have provided core evidence for the dopamine model of schizophrenia and psychosis. The aim of this thesis was to investigate the amphetamine model of schizophrenia by giving 0.45 mg/kg dexamphetamine to healthy volunteers in a double-blind, placebo-controlled, cross-over study who then underwent testing on several electrophysiological endophenotypes of schizophrenia. These measures were, the P3, the 40 Hz auditory steady state response, and prepulse inhibition of the startle reflex. Each of these measures have demonstrated robust deficits in people with schizophrenia. In addition to these electrophysiological measures, a phenomenological correlate of schizophrenia was investigated because a model of psychosis has more face validity if it also induces similar experiential phenomena.
|Qualification||Doctor of Philosophy|
|Publication status||Unpublished - 2012|