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Nicotine withdrawal upregulates nitrergic and galaninergic activity in the rat dorsal raphe nucleus and locus coeruleus
Journal article   Peer reviewed

Nicotine withdrawal upregulates nitrergic and galaninergic activity in the rat dorsal raphe nucleus and locus coeruleus

Chuma O. Okere and Barry D. Waterhouse
Neuroscience letters, v 536(1)
01 Mar 2013
PMID: 23305719

Abstract

Dorsal raphe nucleus Galanin Locus coeruleus Nicotine Nitric oxide synthase
► Nicotine withdrawal increased NOS and galanin staining in DRN subregions and locus coeruleus. ► Nicotine affected more NOS in caudal dorsomedial and lateral wing DRN subregions. ► Nicotine increased both NOS and galanin in specific neurons of rostral ventromedial DRN. ► Nicotine withdrawal stimulates LC-DRN galaninergic neurons. ► NO and galanin synthesized locally in the DRN and LC may mediate the effect of nicotine exposure. The dorsal raphe nucleus (DRN), a major source of forebrain serotonin, mediates various neural functions including anxiety. The nucleus locus coeruleus (LC) is likewise involved in mediating central components of the stress response and anxiety. An anxiety-reducing effect is widely believed to underlie many cases of nicotine dependence. While much is known about nicotine-serotonin interactions, little is known about how nicotine engages the DRN non-serotonergic domain in specific physiological functions that influence organismal behavior. The aim of this study was to determine how chronic nicotine withdrawal influences neuronal nitric oxide (NO) synthase (nNOS) and galanin immunoreactivity in the DRN and LC of adult rats. Compared with saline, nicotine increased nicotinamide adenine dinucleotide phosphate diaphorase profiles within distinct DRN subregions and also enhanced intensity in nNOS and galanin cell bodies in the rostral DRN as well as galanin in the LC. Nicotine-induced nNOS/galanin staining of somata was abundant in the rostral ventromedial DRN. Galanin-positive terminals surrounded nNOS-containing cell bodies in the DRN lateral wing subregions. These observations suggest that the DRN NOS-galanin domain and galanin in the LC are engaged in the organism's neural adaptation to chronic nicotine exposure. Hence NO and galanin synthesized or released within the DRN and LC or at the respective target sites might regulate the whole animal behavioral response to nicotine exposure.

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Domestic collaboration
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Neurosciences
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