Abstract
AbstractEpisodes of mania in bipolar affective disorder patients are associated with a decrease in cerebrospinal fluid calcium. A reduction in extracellular calcium in most neurones leads to a decrease in calcium‐activated potassium conductance mechanisms. Such mechanisms help govern the rate of action potential generation by neurones, and thus the rate of information processing. The dopamine hypothesis of neuroleptic action cannot explain the antimanic actions of lithium, calcium antagonists or carbamazepine. This paper proposes a common mechanism of action for such substances — namely, an action on calcium‐activated potassium conductances.
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