Abstract

Administration of LiCl, 200 mg/kg i.p., to mice twice daily for five to seven doses, led to lower whole brain Na⁺ concentration (P < .05) and higher whole brain Mg⁺⁺ concentration (P < .01) than observed in controls. Lactate production in mouse brain after decapitation was greater in LiCl-treated mice than in saline-injected controls (P < .01). Administration of ouabain before decapitation abolished this increase in lactate production in LiCl-treated mice. Ouabain administration was associated with maintenance of higher levels of adenosine triphosphate (ATP) in brain after decapitation than in controls or in LiCl-treated mice. LiCl administration did not alter ouabain-induced changes in brain ATP after decapitation. In mouse brain, during electrically induced convuLsions, changes in ATP, creatine phosphate, glucose and lactate were no different after administration of LiCl, ouabain or both from those in control mice receiving no drug. This is in contrast to previously reported findings after administration of chlorpromazine, secobarbital anesthesia or anticonvulsant drugs. Brain cations did not change significantly during convulsions. Results are discussed in terms of the relevance to studies of the activity of Na⁺-K⁺-ATPase and their relevance to elucidation of the etiology and treatment of mania.