Acute nicotine treatment attenuates lipopolysaccharide-induced cognitive dysfunction by increasing BDNF expression and inhibiting neuroinflammation in the rat hippocampus. (14th September 2015)

• Record Type: Journal Article
• Authors: Wei, Penghui; Liu, Qingshen; Li, Dong; Zheng, Qiang; Zhou, Jinfeng; Li, Jianjun
• Is Part Of: Neuroscience letters. Volume 604(2015)
• Page Start: 161
• Page End: 166
• Publication Date: 2015-09-14
• Subjects: Acute nicotine treatment -- Lipopolysaccharide (LPS) -- Cognitive dysfunction -- Neuroinflammation -- Brain-derived neurotrophic factor (BDNF); Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2015.08.008
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Acute nicotine treatment ameliorated LPS-induced cognitive dysfunction. Nicotine inhibited the expression of neuroinflammation and apoptosis-related proteins in the dorsal hippocampus. Nicotine increased the expression levels of BDNF in the dorsal hippocampus. Abstract: Although nicotine has been shown to improve cognitive function in various studies, the mechanisms underlying acute nicotine treatment-induced neuroprotection remain incompletely understood. In this study, we evaluated the effect of acute nicotine treatment on the cognitive impairment induced by lipopolysaccharide (LPS) and explored the underlying mechanism. We found that acute nicotine injection markedly attenuated LPS-elicited cognitive deficits and suppressed the strong LPS-induced release of IL-1β, IL-6, and TNF-α into serum and the dorsal hippocampus at 4 and 24 h after LPS injection. Western blot analysis indicated a clear increase in the levels of cleaved caspase-3 in LPS-treated animals but not in nicotine- or saline-treated animals. Furthermore, nicotine administration led to a significant increase in BDNF mRNA expression at 4 and 24 h and in BDNF protein expression at 24 h after LPS injection in the dorsal hippocampus. Taken together, acute nicotine administration attenuated LPS-induced cognitive dysfunction, and this neuroprotective effect may be related to the up-regulation of BDNF and the inhibition of neuroinflammation and apoptosis-related proteins in the dorsal hippocampus.