μ-Opioid receptor in the CA1 involves in tramadol and morphine cross state-dependent memory

• Published in: Neuroscience letters Vol. 705; pp. 177 - 182
• Main Authors: Niknamfar, Saba, Nouri Zadeh-Tehrani, Setareh, Sadat-Shirazi, Mitra-Sadat, Akbarabadi, Ardeshir, Rahimi-Movaghar, Afarin, Zarrindast, Mohammad-Reza
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 13.07.2019
• Subjects: Amnesia - chemically induced; Amnesia - prevention & control; Animals; Avoidance Learning - drug effects; CA1 Region, Hippocampal - drug effects; CA1 Region, Hippocampal - metabolism; Dose-Response Relationship, Drug; Drug Interactions; Male; Memory - drug effects; Mental Recall - drug effects; Microinjections; Morphine; Morphine - pharmacokinetics; Morphine - pharmacology; Naltrexone; Naltrexone - pharmacology; Rats; Receptors, Opioid, mu - agonists; Receptors, Opioid, mu - antagonists & inhibitors; State-dependent memory; Tramadol; Tramadol - antagonists & inhibitors; Tramadol - pharmacology; μ-Opioid receptor; μ-Opioid receptor; State-dependent memory; Morphine; Naltrexone; Tramadol
• DOI: 10.1016/j.neulet.2019.04.054
• ISSN: 0304-3940

•Pre-train tramadol administration (intra-CA1) induced amnesia.•Tramadol administraton in the hippocampus induced state-dependent memory.•Tramadol and morphine had cross state dependent memory.•Tramadol induced state dependent memory regulated via mu-opioid receptor in the CA1. In the present study, the effect of tramadol – an opioid painkiller drug with abuse potential- on amnesia and state-dependent memory and its interaction with the opioidergic system was investigated in male Wistar rats. Intra CA-1 administration of tramadol (0.5, 1, and 2 μg/rat) before training, dose-dependently decreased the learning ability in passive avoidance task. Amnesia induced by pre-train tramadol administration was significantly reversed by pre-test administration of tramadol (1 μg/rat). Pre-test administration of naltrexone (a μ-opioid receptor (MOR) antagonist) inhibited the effect of tramadol on memory retrieval. In addition, the pre-test administration of morphine (1 μg/rat, intra-CA1) also reversed memory impairment induced by pre-train tramadol administration. Although, pre-train morphine administration (1 μg/rat, intra-CA1), induced memory impairment reversed by pre-test tramadol administration (1 μg/rat, intra-CA1). In addition, the level of MOR in the hippocampus decreased in animals with memory impairment due to using tramadol in the training day. However, state-dependent retrieval using tramadol or cross state-dependent retrieval using morphine enhanced the MOR level in the hippocampus. The results of the study suggested that intra-CA1 tramadol administration induced memory impairment, improved by pre-test administration of either tramadol or morphine (MOR agonist). It could be concluded that tramadol is capable to induced state-dependent memory and also, it has a cross state-dependent memory with morphine in the hippocampus, done possibly through MOR.