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Inhibitory role of cholinergic system mediated via 7 nicotinic acetylcholine receptor in LPS-induced neuro-inflammation

Central Drug Research Institute (CDRI)

^* To whom correspondence should be addressed. E-mail: rakeshshukla_cdri{at}rediffmail.com.

	Abstract

This study investigated the influence of the cholinergic system on neuro-inflammation using nicotinic and muscarinic receptor agonists and antagonists. Intracerebroventricular (ICV) injection of lipopolysaccharide (LPS, 50 µg) was used to induce neuro-inflammation in rats and estimations of pro-inflammatory cytokines, 7 nicotinic acetylcholine receptor (nAChR) mRNA expression were done in striatum, cerebral cortex, hippocampus and hypothalamus at 24 h after LPS injection. Nicotine (0.2, 0.4 and 0.8 mg/kg, i.p.) or oxotremorine (0.2, 0.4 and 0.8 mg/kg, i.p.) were administered 2 h prior to sacrifice. We found that only nicotine was able to block the pro-inflammatory cytokines induced by LPS whereas, oxotremorine was found ineffective. Methyllycaconitine (MLA; 1.25, 2.5 and 5 mg/kg, i.p.), an 7 nAChR antagonist or dihydro--erythroidine (DHE; 1.25, 2.5 and 5 mg/kg, i.p.), an 42 nAChR antagonist, was given 20 min prior to nicotine in LPS-treated rats. Methyllycaconitine antagonized the anti-inflammatory effect of nicotine whereas DHE showed no effect demonstrating that 7 nAChR is responsible for attenuation of LPS-induced pro-inflammatory cytokines. This study suggests that the inhibitory role of the central cholinergic system on neuro-inflammation is mediated via 7 nicotinic acetylcholine receptor and muscarinic receptors are not involved.

First published on July 8, 2009
Innate Immunity 2009, doi:10.1177/1753425909104680


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