The amygdala modulates morphine-induced state-dependent memory retrieval via muscarinic acetylcholine receptors

• Published in: Neuroscience 2009-05, Vol.160 (2), p.255-263
• Main Authors: Rezayof, A, Khajehpour, L, Zarrindast, M.R
• Format: Article
• Language: English
• Subjects: Amygdala - drug effects; Amygdala - metabolism; Analgesics; Animals; Association Learning - drug effects; Avoidance Learning - drug effects; Behavior, Animal - drug effects; Biological and medical sciences; Conditioning, Classical - drug effects; Dose-Response Relationship, Drug; Fundamental and applied biological sciences. Psychology; Male; Medical sciences; memory retrieval; Mental Recall - drug effects; Microinjections; Morphine - pharmacology; Muscarinic Antagonists - pharmacology; Narcotics - pharmacology; Neurology; Neuropharmacology; passive avoidance learning; Pharmacology. Drug treatments; pilocarpine; rat; Rats; Rats, Wistar; Receptors, Muscarinic - drug effects; Receptors, Muscarinic - metabolism; Retention (Psychology) - drug effects; scopolamine; Scopolamine Hydrobromide - pharmacology; Vertebrates: nervous system and sense organs
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2009.02.069

Abstract The current study was conducted to examine the involvement of muscarinic acetylcholine receptors of the amygdala in morphine-induced state-dependent memory retrieval. Male Wistar rats implanted bilaterally with cannulas in the amygdala were submitted to a step-through type passive avoidance task, and tested 24 h after training to measure step-through latency. Post-training s.c. administration of morphine at the doses of 5 and 7.5 mg/kg impaired the memory on the test day, which was restored when the same doses of morphine were used as a pre-test drug. This phenomenon is well known as morphine-induced state-dependent memory retrieval. Bilateral microinjection of the non-selective muscarinic acetylcholine receptor agonist, pilocarpine (0.25 and 0.5 μg/side), into the amygdala with an ineffective dose of morphine (0.5 mg/kg s.c.) significantly improved the memory retrieval and mimicked the effects of pre-test administration of a higher dose of morphine. It should be noted that in the animals that received saline after training and tested following intra-amygdala administration of pilocarpine (0.125, 0.25 and 0.5 μg/side) and those which received post-training morphine (7.5 mg/kg s.c.) and pre-test intra-amygdala microinjection of the same doses of pilocarpine, no significant change was observed in the step-through latencies. On the other hand, pre-test intra-amygdala microinjection of a selective muscarinic acetylcholine receptor antagonist scopolamine (0.125 and 0.25 μg/side) inhibited morphine-induced state-dependent memory retrieval. In addition, no significant changes were seen in memory retrieval of the animals trained before saline treatment and tested following intra-amygdala microinjection of the same doses of scopolamine (0.0625, 0.125 and 0.25 μg/side). Bilateral microinjection of scopolamine into the amygdala reversed the pilocarpine-induced potentiation of the morphine response. In view of the known actions of the drugs used, the present data point to the involvement of amygdala muscarinic acetylcholine receptors in morphine-induced state-dependent memory retrieval.