Dorsal Raphe Dual Serotonin-Glutamate Neurons Drive Reward by Establishing Excitatory Synapses on VTA Mesoaccumbens Dopamine Neurons.


Journal

Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691

Informations de publication

Date de publication:
29 01 2019
Historique:
received: 27 06 2018
revised: 12 10 2018
accepted: 03 01 2019
entrez: 31 1 2019
pubmed: 31 1 2019
medline: 14 3 2020
Statut: ppublish

Résumé

Dorsal raphe (DR) serotonin neurons provide a major input to the ventral tegmental area (VTA). Here, we show that DR serotonin transporter (SERT) neurons establish both asymmetric and symmetric synapses on VTA dopamine neurons, but most of these synapses are asymmetric. Moreover, the DR-SERT terminals making asymmetric synapses on VTA dopamine neurons coexpress vesicular glutamate transporter 3 (VGluT3; transporter for accumulation of glutamate for its synaptic release), suggesting the excitatory nature of these synapses. VTA photoactivation of DR-SERT fibers promotes conditioned place preference, elicits excitatory currents on mesoaccumbens dopamine neurons, increases their firing, and evokes dopamine release in nucleus accumbens. These effects are blocked by VTA inactivation of glutamate and serotonin receptors, supporting the idea of glutamate release in VTA from dual DR SERT-VGluT3 inputs. Our findings suggest a path-specific input from DR serotonergic neurons to VTA that promotes reward by the release of glutamate and activation of mesoaccumbens dopamine neurons.

Identifiants

pubmed: 30699344
pii: S2211-1247(19)30022-1
doi: 10.1016/j.celrep.2019.01.014
pmc: PMC6489450
mid: NIHMS1010769
pii:
doi:

Substances chimiques

Amino Acid Transport Systems, Acidic 0
vesicular glutamate transporter 3, mouse 0
Serotonin 333DO1RDJY
Glutamic Acid 3KX376GY7L

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, N.I.H., Intramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1128-1142.e7

Subventions

Organisme : NIGMS NIH HHS
ID : R25 GM060655
Pays : United States
Organisme : NIDA NIH HHS
ID : R01 DA038453
Pays : United States
Organisme : NIMH NIH HHS
ID : R21 MH113341
Pays : United States
Organisme : NIDA NIH HHS
ID : F31 DA041303
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH107229
Pays : United States

Informations de copyright

Published by Elsevier Inc.

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Auteurs

Hui-Ling Wang (HL)

National Institute on Drug Abuse, Neuronal Networks Section, NIH, Baltimore, MD, USA.

Shiliang Zhang (S)

National Institute on Drug Abuse, Electron Microscopy Core, NIH, Baltimore, MD, USA.

Jia Qi (J)

National Institute on Drug Abuse, Neuronal Networks Section, NIH, Baltimore, MD, USA.

Huikun Wang (H)

National Institute on Drug Abuse, Neuronal Networks Section, NIH, Baltimore, MD, USA.

Roger Cachope (R)

Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, MD, USA.

Carlos A Mejias-Aponte (CA)

National Institute on Drug Abuse, Neuronal Networks Section, NIH, Baltimore, MD, USA.

Jorge A Gomez (JA)

Department of Biology, University of Texas at San Antonio, San Antonio, TX, USA.

Gabriel E Mateo-Semidey (GE)

National Institute on Drug Abuse, Neuronal Networks Section, NIH, Baltimore, MD, USA.

Gerard M J Beaudoin (GMJ)

Department of Biology, University of Texas at San Antonio, San Antonio, TX, USA.

Carlos A Paladini (CA)

Department of Biology, University of Texas at San Antonio, San Antonio, TX, USA.

Joseph F Cheer (JF)

Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, MD, USA.

Marisela Morales (M)

National Institute on Drug Abuse, Neuronal Networks Section, NIH, Baltimore, MD, USA. Electronic address: mmorales@intra.nida.nih.gov.

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