[en] Lithium has been suggested for mood disorders and neurodegenerative diseases. Its ability to increase the gray matter and provision of protection against neuronal death makes it tempting to be marketed as brain food. Moreover it also ameliorates the effects of stress on brain dendrites; however lithium has a narrow therapeutic range. Brain serotonin (5-HT) neurotransmission may mediate the actions of lithium. Preclinical studies have shown that single restraint stress produces behavioral and neurochemical deficits. The present study was designed to investigate a potential role of Lithium in attenuation of stress induced behavioral and neurochemical deficits in rats. Moreover the study also monitored the esponsiveness of pre and post synaptic serotonin 1 A receptor following restraint and administration of lithium carbonate. Pre stress behavioral activities were monitored after 15 and 30 days of consumption of 0.1% lithium carbonate in drinking water while post stress were monitored on day 31. Pre and post synaptic 5-HT -1 A responsiveness was monitored by injecting 0.25mg/ml/kg of 8-OH-DPAT. Although lithium produced hypo activity but attenuated stress induced behavioral deficits. Whole brain neurochemical analysis revealed that its administration increased tryptophan, 5-HT and 5-Hydroindoleacetic acid (5-HIAA). 8-OH-DPAT elicited hyperactivity and fore paw treading were enhanced in lithium treated rats. Lithium induced pre synaptic changes together with the super sensitivity of post synaptic receptors may be able to produce antidepressant effect. (author)