Nicotine administration selectively inhibits kainate-induced Arc and junB but not c-fos and egr1 mRNA expression in mouse cerebral cortex.

Abstract

The nicotinic acetylcholine receptor is an ion channel receptor that is highly expressed in the brain and can cooperatively propagate several signals with other ion channel receptors in neurons. However, little is known about how nicotinic acetylcholine and kainate receptors, both of which enable cation influx into neurons, cooperatively regulate immediate early genes. In this study, we administrated both ligands, nicotine and kainate, into mice and investigated alterations of the immediate early genes activity-regulated cytoskeleton-associated protein (Arc), junB, c-fos, and egr1 in the cerebral cortex, hippocampus, olfactory bulb, and cerebellum. Kainate alone showed a tendency to induce all four immediate early genes in all four brain regions, whereas nicotine alone did not induce them strongly. However, pretreatment of nicotine before administration of kainate showed differential effects of nicotine on mRNA expression across different brain regions. Nicotine selectively inhibited kainate-induced Arc and junB mRNA expression in the cerebral cortex. These findings suggest that nicotine influences specific brain regions via the induction of certain immediate early genes.