Chronic but not acute nicotine treatment reverses stress-induced impairment of LTP in anesthetized rats.
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.
Aleisa
A M
AM
Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204-5515, USA.
Alzoubi
K H
KH
Alkadhi
K A
KA
D000758:Anesthesia / Q000379:methods; D000818:Animals; D017774:Long-Term Potentiation / Q000187:drug effects* / Q000502:physiology; D008297:Male; D009538:Nicotine / Q000008:administration & dosage*; D051381:Rats; D017208:Rats, Wistar; D013315:Stress, Psychological / Q000503:physiopathology / Q000517:prevention & control*
D009538:Nicotine