• Hao Zhang, Shao-Bo Zhang, Qing-Qing Zhang, Meng Liu, Xing-Ying He, Zui Zou, Hai-Jing Sun, Zhen-Dong You, and Xue-Yin Shi.
• Department of Anesthesiology and Neuroscience Research Center, Changzheng Hospital, Second Military Medical University, Shanghai, China.
• CNS Neurosci Ther. 2013 Jul 1;19(7):484-93.

AimsThe intravenous anesthetic propofol caused episodic memory impairments in human. We hypothesized propofol caused episodic-like spatial memory retention but not acquisition impairments in rats and rescuing cAMP response element-binding protein (CREB) signaling using selective type IV phosphodiesterase (PDEIV) inhibitor rolipram reversed these effects.MethodsMale Sprague-Dawley rats were randomized into four groups: control; propofol (25 mg/kg, intraperitoneal); rolipram; and rolipram + propofol (pretreatment of rolipram 25 min before propofol, 0.3 mg/kg, intraperitoneal). Sedation and motor coordination were evaluated 5, 15, and 25 min after propofol injection. Invisible Morris water maze (MWM) acquisition and probe test (memory retention) were performed 5 min and 24 h after propofol injection. Visible MWM training was simultaneously performed to resist nonspatial effects. Hippocampal CREB signaling was detected 5 min, 50 min, and 24 h after propofol administration.ResultsRolipram did not change propofol-induced anesthetic/sedative states or impair motor skills. No difference was found on the latency to the platform during the visible MWM. Propofol impaired spatial memory retention but not acquisition. Rolipram reversed propofol-induced spatial memory impairments and suppression on cAMP levels, CaMKIIα and CREB phosphorylation, brain-derived neurotropic factor (BDNF) and Arc protein expression.ConclusionsPropofol caused spatial memory retention impairments but not acquisition inability possibly by inhibiting CREB signaling.© 2013 John Wiley & Sons Ltd.

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