Nicotine prevents stress-induced enhancement of long-term depression in hippocampal area CA1: Electrophysiological and molecular studies

• Published in: Journal of neuroscience research 2006-02, Vol.83 (2), p.309-317
• Main Authors: Aleisa, A.M., Alzoubi, K.H., Alkadhi, K.A.
• Format: Article
• Language: English
• Subjects: Analysis of Variance; Animals; BDNF; Blotting, Western - methods; Brain-Derived Neurotrophic Factor - metabolism; calcineurin; Calcineurin - metabolism; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Calcium-Calmodulin-Dependent Protein Kinases - metabolism; Calmodulin - metabolism; CaMKII; chronic stress; Electric Stimulation - methods; Ganglionic Stimulants - pharmacology; Hippocampus - metabolism; Hippocampus - physiopathology; Long-Term Synaptic Depression - drug effects; Long-Term Synaptic Depression - physiology; Long-Term Synaptic Depression - radiation effects; Male; Nicotine - pharmacology; paired-pulse stimulation; Rats; Rats, Wistar; Stress, Physiological - physiopathology; Time Factors
• ISSN: 0360-4012; 1097-4547
• DOI: 10.1002/jnr.20716

Nicotine treatment prevents chronic psychosocial stress‐induced impairment of hippocampus‐dependent spatial memory and long‐term potentiation (LTP). In this study, we investigated the effect of chronic nicotine treatment on stress‐induced enhancement of long‐term depression (LTD). After paired‐pulse stimulation, LTD was evoked in area CA1 of anesthetized control, stressed, nicotine‐treated, and nicotine‐treated stressed rats. In stressed rats, a significantly greater LTD magnitude was seen than in control rats. Stress also facilitated the induction of LTD. Nicotine treatment of stressed rats prevented stress‐induced enhancement and facilitation of LTD. For chronically stressed rats, we previously reported marked decreases in the basal levels of brain‐derived neurotrophic factor (BDNF), CaMKII, P‐CaMKII, and calmodulin as well as a significant increase in calcineurin basal levels. Herein, Western blot analysis conducted 1 hr after induction of LTD by paired‐pulse stimulation showed that the levels of calcineurin and P‐CaMKII were increased in the stressed group compared with the other groups and were normalized by chronic nicotine treatment. Additionally, after paired‐pulse stimulation, the levels of total CaMKII were increased in all groups with no change in the levels of BDNF and calmodulin. Therefore, the increase in the levels of calcineurin and P‐CaMKII during expression of LTD in area CA1 may explain the enhanced magnitude of LTD in chronically stressed rats. © 2005 Wiley‐Liss, Inc.