Abstract
Background: Bipolar disorder type I is a severe psychiatric condition that leads to significant morbidity and mortality and whose treatment remains suboptimal. Its pathophysiology involves disturbance in the control of ionic fluxes so that when patients are either manic or depressed, the resting membrane potential of neurons is more depolarized than normal. Available mood stabilizers have a shared mechanism of normalizing ion flux by compensating for ionic abnormalities, and normalizing membrane potential.