• Mehdi Ghasemi, Hamed Sadeghipour, Gholamreza Poorheidari, and Ahmad Reza Dehpour.
• Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, P.O. Box 13145-784, Tehran, Iran. m82 ghsemi@yahoo.com
• Behav. Brain Res. 2009 Jun 8; 200 (1): 76-82.

AbstractIn the present study we evaluated the involvement of nitric oxide (NO) system in the antidepressant-like effects of chronic lithium administration in the mouse forced swimming test (FST). Administration of lithium chloride (300 mg/L in drinking water for 21 days) had no effect on the immobility of mice in the FST, whereas 600 mg/L lithium caused a significant (P<0.001) decrease in the immobility time compared with control animals. Administration of the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 10mg/kg, daily for a week, i.p.) had no significant effect on the immobility time of either control or lithium (300 mg/L)-treated mice, whereas acute administration of non-effective dose of L-NAME (30 mg/kg, i.p.) caused a robust decrease (P<0.01) in the immobility time of lithium (300 mg/L)-treated animals in the FST. Moreover, chronic administration of low dose of the NO precursor L-arginine (200 mg/kg, daily for a week, i.p.) prevented (P<0.001) the antidepressant-like effects of lithium treatment (600 mg/L) in the FST. Acute treatment with L-arginine (200 mg/kg, i.p.) increased (P<0.05) the immobility time of lithium (600 mg/L)-treated mice in the FST. Chronic lithium treatment (600 mg/L but not 300 mg/L) caused a significant (P<0.05) decrease in the serum NO(X) levels in mice compared with controls. Our data suggested that the NO system could be involved in the antidepressant-like effect of chronic lithium treatment in the FST.

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