Participation of hippocampal nicotinic receptors in acquisition, consolidation and retrieval of memory for one trial inhibitory avoidance in rats

• Published in: Neuroscience Vol. 126; no. 3; pp. 651 - 656
• Main Authors: Martí Barros, D., Ramirez, M.R., dos Reis, E.A., Izquierdo, I.
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 2004; Elsevier
• Subjects: Animals; Avoidance Learning - drug effects; Avoidance Learning - physiology; Biological and medical sciences; dihydro-beta-erythroidine; Fundamental and applied biological sciences. Psychology; hippocampus; Hippocampus - drug effects; Hippocampus - metabolism; Injections, Intraventricular; Male; Maze Learning - drug effects; Maze Learning - physiology; mecamylamine; memory; Memory - drug effects; Memory - physiology; nicotine; Nicotinic Agonists - administration & dosage; Nicotinic Antagonists - administration & dosage; Rats; Rats, Wistar; Receptors, Nicotinic - drug effects; Receptors, Nicotinic - metabolism; Vertebrates: nervous system and sense organs; mecamylamine; nicotine; memory; hippocampus; LTM; nAChR; DHβE; STM; dihydro-beta-erythroidine; Memory retrieval; Rat; Memory; Rodentia; Central nervous system; Encephalon; Cholinergic receptor; Vertebrata; Mammalia; Animal; Nicotinic receptor; Avoidance; Hippocampus
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2004.03.010

One-trial step-down inhibitory avoidance in rats involves the activation of two separate memory types, a short-term system (STM) that lasts 3–6 h, and a long-term system (LTM) that takes 3–6 h to be formed and lasts for many days or even months. Here we investigate the effect of nicotinic receptor (nAChR) ligands infused bilaterally in the hippocampus on STM and LTM formation and on LTM retrieval of this task. Rats were implanted with chronic cannulae in the CA1 region of the dorsal hippocampus, trained using a 0.5 mA foot shock, and tested twice, first 1.5 h after training to measure STM, and again at 24 h to measure LTM. The drugs used were the nAChR antagonists, mecamylamine (1, 3 and 10 μg/side) and dihydro-β-erythroidine (DHβE; 2, 6 and 18 μg/side) and the agonist, nicotine (0.6, 1 and 3 μg/side). They were given either 15 min before training, immediately after training or 15 min prior to LTM retrieval. Mecamylamine and DHβE impaired and nicotine enhanced STM, LTM and retrieval similarly. The results indicate that nAChRs in CA1 participate in the regulation of both STM and LTM formation, and on the retrieval of LTM.