The acute inhibition of rapid eye movement sleep by citalopram may impair spatial learning and passive avoidance in mice

• Published in: Journal of Neural Transmission Vol. 120; no. 3; pp. 383 - 389
• Main Authors: Bridoux, A., Laloux, C., Derambure, P., Bordet, R., Monaca Charley, C.
• Format: Journal Article
• Language: English
• Published: Vienna Springer Vienna 01-03-2013; Springer Nature B.V
• Subjects: Animals; Avoidance learning; Avoidance Learning - drug effects; citalopram; Citalopram - administration & dosage; Citalopram - toxicity; Cognitive ability; Male; Maze Learning - drug effects; Medicine; Medicine & Public Health; Memory; Memory - drug effects; Mice; Mice, Inbred C57BL; Neurology; Neurosciences; Polysomnography; Psychiatry; Serotonin uptake inhibitors; Serotonin Uptake Inhibitors - administration & dosage; Serotonin Uptake Inhibitors - toxicity; Sleep (REM); Sleep Deprivation - chemically induced; Sleep Deprivation - complications; Sleep, REM - drug effects; Spatial discrimination learning; spatial memory; Translational Neurosciences - Original Article; Memory; Passive avoidance; Sleep deprivation; REM sleep; Citalopram; Y-maze
• ISSN: 0300-9564; 1435-1463
• DOI: 10.1007/s00702-012-0901-0

Rapid eye movement (REM) sleep is known to be essential for memory. Hence, REM sleep deprivation impairs memory processes. The frequently prescribed selective serotonin reuptake inhibitors (SSRIs) are known to cause REM sleep deprivation and to impair cognitive performance in humans and rodents. We suggested that impaired memory processes by citalopram in C57/BL6 mice could be explained by the acute inhibition of REM sleep. We hypothesized that those acute citalopram 5 and 10 mg/kg injections induced REM sleep deprivation, altered cognitive performance in passive avoidance, impaired spatial memory compared to controls. Three experiments have been realized: (1) mice received successively physiological saline, injection of citalopram 5 and 10 mg/kg and were recorded by polysomnographic recording after each injection. (2) Cognitive performance was evaluated in the passive avoidance with two groups of mice. One group received citalopram before training and one, after training. (3) Spatial learning was evaluated with another group of animals in the Y-maze test. At 5 and 10 mg/kg, citalopram delayed REM sleep onset and decreased REM sleep amounts (vs. controls). The same doses were administrated in the passive avoidance test and have significantly shortened latency to enter the dark compartment. In the Y-maze, citalopram-treated mice showed a decreased percentage of time spent in the novel arm in contrast to the two other arms compared with controls. We showed that citalopram impaired cognitive performance in behavioral tasks. Those impairments could be linked to REM sleep deprivation induced by citalopram although causal relationship needs to be investigated in further studies.