Nicotinic receptors mediate stress-nicotine detrimental interplay via dopamine cells' activity

C Morel; S P Fernandez; F Pantouli; F J Meye; F Marti; S Tolu; S Parnaudeau; H Marie; F Tronche; U Maskos; M Moretti; C Gotti; M-H Han; A Bailey; M Mameli; J Barik; P Faure

doi:10.1038/mp.2017.145

Nicotinic receptors mediate stress-nicotine detrimental interplay via dopamine cells' activity

C Morel, S P Fernandez, F Pantouli, F J Meye, F Marti, S Tolu, S Parnaudeau, H Marie, F Tronche, U Maskos, M Moretti, C Gotti, M-H Han, A Bailey, M Mameli, J Barik, P Faure

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

Epidemiological studies report strong association between mood disorders and tobacco addiction. This high comorbidity requires adequate treatment but the underlying mechanisms are unknown. We demonstrate that nicotine exposure, independent of drug withdrawal effects, increases stress sensitivity, a major risk factor in mood disorders. Nicotine and stress concur to induce long-lasting cellular adaptations within the dopamine (DA) system. This interplay is underpinned by marked remodeling of nicotinic systems, causing increased ventral tegmental area (VTA) DA neurons' activity and stress-related behaviors, such as social aversion. Blocking β2 or α7 nicotinic acetylcholine receptors (nAChRs) prevents, respectively, the development and the expression of social stress-induced neuroadaptations; conversely, facilitating α7 nAChRs activation specifically in the VTA promotes stress-induced cellular and behavioral maladaptations. Our work unravels a complex nicotine-stress bidirectional interplay and identifies α7 nAChRs as a promising therapeutic target for stress-related psychiatric disorders.

Original language	English
Pages (from-to)	1597-1605
Number of pages	9
Journal	Molecular Psychiatry
Volume	23
Issue number	7
DOIs	https://doi.org/10.1038/mp.2017.145
Publication status	Published - 1 Jul 2018
Externally published	Yes

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Morel, C., Fernandez, S. P., Pantouli, F., Meye, F. J., Marti, F., Tolu, S., Parnaudeau, S., Marie, H., Tronche, F., Maskos, U., Moretti, M., Gotti, C., Han, M.-H., Bailey, A., Mameli, M., Barik, J., & Faure, P. (2018). Nicotinic receptors mediate stress-nicotine detrimental interplay via dopamine cells' activity. Molecular Psychiatry, 23(7), 1597-1605. https://doi.org/10.1038/mp.2017.145

@article{ad9677dae464464fa034334fb4b8682a,

title = "Nicotinic receptors mediate stress-nicotine detrimental interplay via dopamine cells' activity",

abstract = "Epidemiological studies report strong association between mood disorders and tobacco addiction. This high comorbidity requires adequate treatment but the underlying mechanisms are unknown. We demonstrate that nicotine exposure, independent of drug withdrawal effects, increases stress sensitivity, a major risk factor in mood disorders. Nicotine and stress concur to induce long-lasting cellular adaptations within the dopamine (DA) system. This interplay is underpinned by marked remodeling of nicotinic systems, causing increased ventral tegmental area (VTA) DA neurons' activity and stress-related behaviors, such as social aversion. Blocking β2 or α7 nicotinic acetylcholine receptors (nAChRs) prevents, respectively, the development and the expression of social stress-induced neuroadaptations; conversely, facilitating α7 nAChRs activation specifically in the VTA promotes stress-induced cellular and behavioral maladaptations. Our work unravels a complex nicotine-stress bidirectional interplay and identifies α7 nAChRs as a promising therapeutic target for stress-related psychiatric disorders.",

author = "C Morel and Fernandez, {S P} and F Pantouli and Meye, {F J} and F Marti and S Tolu and S Parnaudeau and H Marie and F Tronche and U Maskos and M Moretti and C Gotti and M-H Han and A Bailey and M Mameli and J Barik and P Faure",

note = "Funding Information: This work was supported by the CNRS UMR 8246, Institut Universitaire de France to JB, the Foundation for Medical Research (FRM, Equipe DEQ20130326488 to PF), ANR (ANR-13-JSV4-0004 to JB, ANR-16 Nicostress to PF and JB), the Bettencourt Schueller Foundation (Coup d'Elan 2012 to PF), the Labex Bio-Psy, the Institut National du Cancer to JB, UM and PF, the {\textquoteleft}SmokeFreeBrain Horizon 2020 grant (No681120){\textquoteright} to AB, and the National Institute on Alcohol Abuse and Alcoholism (AA022445), the National Institute of Mental Health (MH112081), the NARSAD Independent Investigator Award to MHH. The laboratories of MM and PF are part of the {\'E}cole des Neurosciences de Paris Ile-de-France RTRA network. MM and PF are members of the Laboratory of Excellence, LabEx Bio-Psy. PF is a member of DHU Pepsy. Publisher Copyright: {\textcopyright} 2018, Springer Nature Limited.",

year = "2018",

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doi = "10.1038/mp.2017.145",

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volume = "23",

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Morel, C, Fernandez, SP, Pantouli, F, Meye, FJ, Marti, F, Tolu, S, Parnaudeau, S, Marie, H, Tronche, F, Maskos, U, Moretti, M, Gotti, C, Han, M-H, Bailey, A, Mameli, M, Barik, J & Faure, P 2018, 'Nicotinic receptors mediate stress-nicotine detrimental interplay via dopamine cells' activity', Molecular Psychiatry, vol. 23, no. 7, pp. 1597-1605. https://doi.org/10.1038/mp.2017.145

TY - JOUR

T1 - Nicotinic receptors mediate stress-nicotine detrimental interplay via dopamine cells' activity

AU - Morel, C

AU - Fernandez, S P

AU - Pantouli, F

AU - Meye, F J

AU - Marti, F

AU - Tolu, S

AU - Parnaudeau, S

AU - Marie, H

AU - Tronche, F

AU - Maskos, U

AU - Moretti, M

AU - Gotti, C

AU - Han, M-H

AU - Bailey, A

AU - Mameli, M

AU - Barik, J

AU - Faure, P

N1 - Funding Information: This work was supported by the CNRS UMR 8246, Institut Universitaire de France to JB, the Foundation for Medical Research (FRM, Equipe DEQ20130326488 to PF), ANR (ANR-13-JSV4-0004 to JB, ANR-16 Nicostress to PF and JB), the Bettencourt Schueller Foundation (Coup d'Elan 2012 to PF), the Labex Bio-Psy, the Institut National du Cancer to JB, UM and PF, the ‘SmokeFreeBrain Horizon 2020 grant (No681120)’ to AB, and the National Institute on Alcohol Abuse and Alcoholism (AA022445), the National Institute of Mental Health (MH112081), the NARSAD Independent Investigator Award to MHH. The laboratories of MM and PF are part of the École des Neurosciences de Paris Ile-de-France RTRA network. MM and PF are members of the Laboratory of Excellence, LabEx Bio-Psy. PF is a member of DHU Pepsy. Publisher Copyright: © 2018, Springer Nature Limited.

PY - 2018/7/1

Y1 - 2018/7/1

N2 - Epidemiological studies report strong association between mood disorders and tobacco addiction. This high comorbidity requires adequate treatment but the underlying mechanisms are unknown. We demonstrate that nicotine exposure, independent of drug withdrawal effects, increases stress sensitivity, a major risk factor in mood disorders. Nicotine and stress concur to induce long-lasting cellular adaptations within the dopamine (DA) system. This interplay is underpinned by marked remodeling of nicotinic systems, causing increased ventral tegmental area (VTA) DA neurons' activity and stress-related behaviors, such as social aversion. Blocking β2 or α7 nicotinic acetylcholine receptors (nAChRs) prevents, respectively, the development and the expression of social stress-induced neuroadaptations; conversely, facilitating α7 nAChRs activation specifically in the VTA promotes stress-induced cellular and behavioral maladaptations. Our work unravels a complex nicotine-stress bidirectional interplay and identifies α7 nAChRs as a promising therapeutic target for stress-related psychiatric disorders.

AB - Epidemiological studies report strong association between mood disorders and tobacco addiction. This high comorbidity requires adequate treatment but the underlying mechanisms are unknown. We demonstrate that nicotine exposure, independent of drug withdrawal effects, increases stress sensitivity, a major risk factor in mood disorders. Nicotine and stress concur to induce long-lasting cellular adaptations within the dopamine (DA) system. This interplay is underpinned by marked remodeling of nicotinic systems, causing increased ventral tegmental area (VTA) DA neurons' activity and stress-related behaviors, such as social aversion. Blocking β2 or α7 nicotinic acetylcholine receptors (nAChRs) prevents, respectively, the development and the expression of social stress-induced neuroadaptations; conversely, facilitating α7 nAChRs activation specifically in the VTA promotes stress-induced cellular and behavioral maladaptations. Our work unravels a complex nicotine-stress bidirectional interplay and identifies α7 nAChRs as a promising therapeutic target for stress-related psychiatric disorders.

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U2 - 10.1038/mp.2017.145

DO - 10.1038/mp.2017.145

M3 - Article

C2 - 29155800

SN - 1359-4184

VL - 23

SP - 1597

EP - 1605

JO - Molecular Psychiatry

JF - Molecular Psychiatry

IS - 7

ER -

Nicotinic receptors mediate stress-nicotine detrimental interplay via dopamine cells' activity

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