Up-regulation of the D1 Dopamine Receptor–Interacting Protein, Calcyon, in Patients With Schizophrenia

Abstract
THE DOPAMINE hypothesis continues to guide biological research in schizophrenia despite difficulties in identifying a clear disease-associated abnormality in the presynaptic or postsynaptic components of the brain's dopamine system.1- 4 This hypothesis is founded in large part on the therapeutic efficacy of antipsychotic medications, universally attributed to their action at D2 dopamine receptors.2,5- 7 It has been argued that antipsychotic drug treatment may also affect D1 dopamine receptors.2,6,8- 12 Furthermore, D1 receptor involvement in schizophrenia is suggested by the ability of D1 receptor–acting drugs to alter working memory performance,6,10,13- 19 an abnormality that is now widely recognized to be a core feature of schizophrenia.6,13,14,20,21 Both suppression and overstimulation of D1 receptor activity have been shown to result in working memory deficits.15