Chronic but not acute nicotine treatment reverses stress-induced impairment of LTP in anesthetized rats.

Abstract

Stress impairs long-term potentiation (LTP) and is a major cause for starting or increasing tobacco smoking. We have previously shown that chronic concurrent nicotine treatment prevents stress-induced LTP impairment. Nicotine reduces stress-induced impairment of LTP, probably, through activation of nicotinic acetylcholine receptors in the hippocampus. Herein, we investigated the effects of acute and chronic nicotine treatments on the chronic-stress-induced impairment of LTP in area CA1 of the hippocampus of urethane-anesthetized rats. Extracellular in vivo recording from the hippocampal area CA1 showed that pre-treatment with nicotine (1 mg/kg; sc twice/day for 2 weeks prior to stress) protected LTP from the inhibitory effect of subsequent chronic psychosocial stress (4 additional weeks concurrently with nicotine). In another series of experiments, 2 weeks of psychosocial stress was followed by 4 weeks of nicotine treatment concurrently with continuing stress. Nicotine treatment reversed established stress-induced impairment of LTP. However, acute nicotine treatment of rats (a single dose of 1 mg/kg; sc.) did not reverse chronic-stress-induced impairment of LTP. The results show that the impairment of LTP during chronic stress can be blocked by chronic, but not acute, nicotine treatment.