alexa The Sensory Impact of Nicotine on Noradrenergic and Dopaminergic Neurons of the Nicotine Reward - Addiction Neurocircuitry | OMICS International | Abstract
ISSN: 2155-6105

Journal of Addiction Research & Therapy
Open Access

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Research Article

The Sensory Impact of Nicotine on Noradrenergic and Dopaminergic Neurons of the Nicotine Reward - Addiction Neurocircuitry

Jed E Rose1, Ozra Dehkordi2,3*, Kebreten F Manaye3, Richard M Millis4, Salman Ameri Cianaki2 and Annapurni Jayam-Trouth2

1Department of Psychiatry, Duke University Medical Centre, Durham, N.C. 27705, United States

2Department of Neurology, Howard University Hospital, Washington, D.C. 20060, United States

3Department of Physiology & Biophysics, Howard University College of Medicine, Washington, D.C. 20059, United States

4Department of Medical Physiology, American University of Antigua College of Medicine, St. John’s, Antigua and Barbuda

Corresponding Author:
Dehkordi Ozra
Associate Professor, Department of Neurology
Howard University Hospital, Washington, United States
Tel: +1 202 865 1978
Fax: +1 202 865 1977
E-mail: [email protected]

Received date: Feb 16, 2016; Accepted date: April 01, 2016; Published date: April 07, 2016

Citation: Rose JE, Dehkordi O, Manaye KF, Millis RM, Cianaki SA, et al. (2016) The Sensory Impact of Nicotine on Noradrenergic and Dopaminergic Neurons of the Nicotine Reward - Addiction Neurocircuitry. J Addict Res Ther 7:274. doi:10.4172/2155-6105.1000274

Copyright: © 2016 Rose JE, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


The sensory experience of smoking is a key component of nicotine addiction known to result, in part, from stimulation of nicotinic acetylcholine receptors (nAChRs) at peripheral sensory nerve endings. Such stimulation of nAChRs is followed by activation of neurons at multiple sites in the mesocorticolimbic reward pathways. However, the neurochemical profiles of CNS cells that mediate the peripheral sensory impact of nicotine remain unknown. In the present study in mice, we first used c-Fos immunohistochemistry to identify CNS cells stimulated by nicotine (NIC, 40 μg/kg, IP) and by a peripherally-acting analog of nicotine, nicotine pyrrolidine methiodide (NIC-PM, 30 μg/kg, IP). Sequential double-labelling was then performed to determine whether noradrenergic and dopaminergic neurons of the nicotine reward-addiction circuitry were primary targets of NIC and NIC-PM. Double-labelling of NIC and/or NIC-PM activated c-Fos immunoreactive cells with tyrosine hydroxylase (TH) showed no apparent c-Fos expression by the dopaminergic cells of the ventral tegmental area (VTA). With the exception of sparse numbers of TH immunoreactive D11 cells, dopamine-containing neurons in other areas of the reward-addiction circuitry, namely periaqueductal gray, and dorsal raphe, were also devoid of c-Fos immune-reactivity. Noradrenergic neurons of locus coeruleus (LC), known to innervate VTA, were activated by both NIC and NIC-PM. These results demonstrate that noradrenergic neurons of LC are among the first structures that are stimulated by single acute IP injection of NIC and NIC-PM. Dopaminergic neurons of VTA and other CNS sites, did not respond to acute IP administration of NIC or NIC-PM by induction of c-Fos.