Activation of septal OXTr neurons induces anxiety- but not depressive-like behaviors.


Journal

Molecular psychiatry
ISSN: 1476-5578
Titre abrégé: Mol Psychiatry
Pays: England
ID NLM: 9607835

Informations de publication

Date de publication:
12 2021
Historique:
received: 16 02 2021
accepted: 25 08 2021
revised: 14 08 2021
pubmed: 8 9 2021
medline: 15 3 2022
entrez: 7 9 2021
Statut: ppublish

Résumé

The neuropeptide oxytocin (OXT) is well recognized for eliciting anxiolytic effects and promoting social reward. However, emerging evidence shows that OXT increases aversive events. These seemingly inconsistent results may be attributable to the broad OXT receptor (OXTr) expression in the central nervous system. This study selectively activated septal neurons expressing OXTr using chemogenetics. We found that chemogenetic activation of septal OXTr neurons induced anxiety- but not depressive-like behavior. In addition, septal OXTr neurons projected dense fibers to the horizontal diagonal band of Broca (HDB), and selective stimulation of those HDB projections also elicited anxiety-like behaviors. We also found that septal OXTr neurons express the vesicular GABA transporter (vGAT) protein and optogenetic stimulation of septal OXTr projections to the HDB inactivated HDB neurons. Our data collectively reveal that septal OXTr neurons increase anxiety by projecting inhibitory GABAergic inputs to the HDB.

Identifiants

pubmed: 34489531
doi: 10.1038/s41380-021-01283-y
pii: 10.1038/s41380-021-01283-y
pmc: PMC8873014
mid: NIHMS1735976
doi:

Substances chimiques

Receptors, Oxytocin 0
Oxytocin 50-56-6

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

7270-7279

Subventions

Organisme : NICHD NIH HHS
ID : P50 HD105352
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK112759
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH109441
Pays : United States

Informations de copyright

© 2021. The Author(s).

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Auteurs

Tuanjie Huang (T)

Department of Medicine Division of Endocrinology, Albert Einstein College of Medicine, Bronx, NY, USA.
School of Life Sciences, Zhengzhou University, Zhengzhou, Henan, China.

Fangxia Guan (F)

School of Life Sciences, Zhengzhou University, Zhengzhou, Henan, China.

Julio Licinio (J)

Departments of Psychiatry and Neuroscience, SUNY Upstate Medical University, Syracuse, NY, USA.

Ma-Li Wong (ML)

Departments of Psychiatry and Neuroscience, SUNY Upstate Medical University, Syracuse, NY, USA.

Yunlei Yang (Y)

Department of Medicine Division of Endocrinology, Albert Einstein College of Medicine, Bronx, NY, USA. yunlei.yang@einsteinmed.org.
Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY, USA. yunlei.yang@einsteinmed.org.
Einstein-Mount Sinai Diabetes Research Center, Albert Einstein College of Medicine, Bronx, NY, USA. yunlei.yang@einsteinmed.org.
The Fleischer Institute for Diabetes and Metabolism, Albert Einstein College of Medicine, Bronx, NY, USA. yunlei.yang@einsteinmed.org.

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