Chronic psychosocial stress-induced impairment of hippocampal LTP: Possible role of BDNF

Electrophysiological recording reveals that chronic nicotine treatment prevents stress-induced impairment of long-term potentiation (LTP) in the CA1 region of the hippocampus of anesthetized rats. We investigated the molecular mechanism of this action of nicotine in the CA1 region. Immunoblot analys...

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Bibliographic Details
Published in:Neurobiology of disease 2006-06, Vol.22 (3), p.453-462
Main Authors: Aleisa, A.M., Alzoubi, K.H., Gerges, N.Z., Alkadhi, K.A.
Format: Article
Language:English
Subjects:
Anesthetized rat
Animals
Blotting, Western
Brain-Derived Neurotrophic Factor - drug effects
CA1 region
Calcineurin
Calcineurin - drug effects
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Calcium-Calmodulin-Dependent Protein Kinases - drug effects
Calmodulin - drug effects
CaMKII
Electric Stimulation
Excitatory Postsynaptic Potentials - drug effects
fEPSP
Ganglionic Stimulants - pharmacology
Hippocampus - drug effects
Long-Term Potentiation - drug effects
Long-Term Potentiation - physiology
Male
Nicotine - pharmacology
Population spike
Psychology
Rats
Rats, Wistar
Stress, Psychological - physiopathology
Stress, Psychological - prevention & control
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Summary:Electrophysiological recording reveals that chronic nicotine treatment prevents stress-induced impairment of long-term potentiation (LTP) in the CA1 region of the hippocampus of anesthetized rats. We investigated the molecular mechanism of this action of nicotine in the CA1 region. Immunoblot analysis showed that chronic nicotine treatment (1 mg/kg, 2 times/day) normalized the stress-induced decrease in the basal levels of BDNF, CaMKII (total and phosphorylated; P-CaMKII), and calmodulin. Additionally, nicotine reversed the stress-induced increase in calcineurin basal levels. Chronic nicotine treatment also markedly increased the basal levels of BDNF in naïve rats. Furthermore, high-frequency stimulation (HFS), which increased the levels of P-CaMKII in control as well as nicotine-treated stressed rats, failed to increase P-CaMKII levels in untreated stressed rats. Compared to unstimulated control, the levels of both total CaMKII and calcineurin were increased after HFS in all groups including the stressed, but no changes were detected after HFS in the levels of BDNF and calmodulin. These results indicate that normalization by nicotine of the stress-induced changes in the levels of signaling molecules including BDNF may contribute to the recovery of LTP.
ISSN:0969-9961
1095-953X
DOI:10.1016/j.nbd.2005.12.005