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Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury
Published on: November 19, 2012
Chronic intermittent nicotine administration attenuates traumatic brain injury-induced cognitive dysfunction
S L Verbois1, D M Hopkins, S W Scheff
1Division of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, KY 40536-0082, USA.
Neuroscience
|July 2, 2003
Summary
Nicotine injections improved cognitive function after traumatic brain injury (TBI) in rats. This effect was observed despite no significant changes in alpha7* nicotinic acetylcholine receptors, suggesting a role for other receptor subtypes.
Area of Science:
- Neuroscience
- Pharmacology
- Trauma Research
Background:
- Traumatic brain injury (TBI) causes neuropathological changes and cognitive deficits.
- TBI is associated with decreased central nervous system (CNS) alpha7* nicotinic acetylcholine receptors (nAChRs).
Purpose of the Study:
- To determine if nicotine administration can improve cognitive performance following experimental TBI.
- To investigate the role of alpha7* nAChRs in nicotine's potential therapeutic effects after TBI.
Main Methods:
- Adult male rats received controlled cortical impact (CCI) TBI.
- Animals were administered nicotine injections pre-injury, post-injury, or both.
- Cognitive performance was assessed using the Morris water maze (MWM).
- nAChR expression was evaluated via receptor binding assays.
Main Results:
- Nicotine treatment post-injury attenuated TBI-induced cognitive deficits in the MWM.
- Nicotine did not significantly alter the TBI-induced decrease in alpha7* nAChR expression.
- Nicotine up-regulated non-alpha7* nAChRs, potentially mitigating TBI-related deficits.
Conclusions:
- Nicotine administration is effective in improving cognitive deficits after TBI.
- The therapeutic effects of nicotine may be mediated by non-alpha7* nAChRs, independent of alpha7* nAChR modulation.
