Rona J Roberts1, Richard Repass, Rif S El-Mallakh. 1. Mood Disorders Research Program, Department of Psychiatry and Behavioral Sciences, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Abstract
BACKGROUND: The pathogenesis of bipolar illness is unknown. A search for common mechanism of action in effective medications has been utilized as a method to gain clues into mechanisms of illness. The recent increase of reports of documented efficacy of first- and second-generation antipsychotics in the control of mania offers a new opportunity to gain insight into the pathophysiological mechanism of bipolar disorder. METHODS: A selected critical review of the literature is performed to gain insights into the effect of antipsychotic medications on ion regulation. RESULTS: Dopamine D(1) and D(2) receptor stimulation increases intracellular sodium concentrations. D(1) and D(2) blockade normalizes stimulated intracellular sodium concentrations, and increases active sodium pump expression. CONCLUSIONS: A similar exercise has previously suggested that lithium and effective anticonvulsants reduce sodium influx in an activity-dependent manner. The current review suggests that antipsychotic medications may have a similar effect by a different mechanism. The role of ion dysregulation in the genesis of mania in bipolar illness needs to continue to be examined.
BACKGROUND: The pathogenesis of bipolar illness is unknown. A search for common mechanism of action in effective medications has been utilized as a method to gain clues into mechanisms of illness. The recent increase of reports of documented efficacy of first- and second-generation antipsychotics in the control of mania offers a new opportunity to gain insight into the pathophysiological mechanism of bipolar disorder. METHODS: A selected critical review of the literature is performed to gain insights into the effect of antipsychotic medications on ion regulation. RESULTS:Dopamine D(1) and D(2) receptor stimulation increases intracellular sodium concentrations. D(1) and D(2) blockade normalizes stimulated intracellular sodium concentrations, and increases active sodium pump expression. CONCLUSIONS: A similar exercise has previously suggested that lithium and effective anticonvulsants reduce sodium influx in an activity-dependent manner. The current review suggests that antipsychotic medications may have a similar effect by a different mechanism. The role of ion dysregulation in the genesis of mania in bipolar illness needs to continue to be examined.