The effect of citalopram treatment on memory performance, mood state, catalase, BDNF, and MDA in REM sleep-deprived rats.

Rapid-eye movement (REM) sleep is a critical stage of sleep that plays a pivotal role in memory formation, consolidation, and mood regulation. While REM sleep deprivation (REM SD) has been shown to impair cognitive and affective functions, findings across studies remain inconsistent. REM SD may also influence the expression of brain-derived neurotrophic factor (BDNF), a key protein involved in memory and mood-related processes. In this study, we investigated the effects of REM SD (6 h/day for 7 days) on behavioral and cognitive performance, BDNF levels in the prefrontal cortex, and serum markers of oxidative stress-catalase (CAT, an antioxidant enzyme) and malondialdehyde (MDA, a lipid peroxidation product). Additionally, we evaluated the potential therapeutic effect of citalopram (20 mg/kg, i.p., for 7 days) on REM SD-induced behavioral deficits. Our results demonstrated that REM SD increased locomotor activity and rearing behavior, impaired passive avoidance memory, and reduced pain threshold. REM SD also downregulated prefrontal BDNF expression but did not alter serum CAT or MDA levels. Citalopram treatment reversed REM SD-induced hyperlocomotion, increased rearing, pain hypersensitivity, and BDNF downregulation; however, it did not significantly improve memory impairment. Depressive-like behavior remained unchanged across groups. These findings suggest that BDNF modulation may underlie both the detrimental effects of REM SD and the therapeutic actions of citalopram, whereas peripheral oxidative stress markers (CAT and MDA) do not appear to play a major role in this paradigm.