Oxytocinergic input from the paraventricular nucleus to the nucleus accumbens core modulates methamphetamine-conditioned place preference

Abstract Methamphetamine (METH) is a highly addictive psychostimulant, yet its addiction mechanisms remain unclear. Oxytocin (OXT), a neuropeptide, shows promise in reducing METH addiction, but how OXT exerts its effects is poorly understood. Using conditioned place preference (CPP), we first found...

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Main Authors: Ying-jie Cheng, Gui-ying Zan, Ying-zhi Deng, Di Deng, Man-qing Wu, Jing-rui Chai, Yu-jun Wang, Jing-gen Liu, Min Zhao
Format: Article
Language:English
Published: Nature Portfolio 2025-05-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-59859-z
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author Ying-jie Cheng
Gui-ying Zan
Ying-zhi Deng
Di Deng
Man-qing Wu
Jing-rui Chai
Yu-jun Wang
Jing-gen Liu
Min Zhao
author_facet Ying-jie Cheng
Gui-ying Zan
Ying-zhi Deng
Di Deng
Man-qing Wu
Jing-rui Chai
Yu-jun Wang
Jing-gen Liu
Min Zhao
author_sort Ying-jie Cheng
collection DOAJ
description Abstract Methamphetamine (METH) is a highly addictive psychostimulant, yet its addiction mechanisms remain unclear. Oxytocin (OXT), a neuropeptide, shows promise in reducing METH addiction, but how OXT exerts its effects is poorly understood. Using conditioned place preference (CPP), we first found that intranasal OXT other than Arginine Vasopressin (AVP) administration suppressed METH-CPP in mice, which could be reversed by OXT receptors (OXTRs) blockade in the nucleus accumbens (NAc) core. Activating OXTRs in the NAc core similarly reduced METH-CPP. Then, we found repeated METH exposure inhibited oxytocinergic neurons within the paraventricular nucleus (PVN) and lowered PVN OXT protein level. Chemogenetic activation of PVN oxytocinergic neurons (PVNOXT) blocked METH-CPP. Furthermore, METH inhibited PVNOXT-NAc core circuit other than PVNOXT-NAc shell circuit. Activation of PVNOXT-NAc core circuit significantly inhibited METH-CPP. This study reveals METH may impair the endogenous OXT system, especially the PVNOXT-NAc core circuit, highlighting OXT’s therapeutic potential for METH use disorder (MUD).
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institution Kabale University
issn 2041-1723
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publishDate 2025-05-01
publisher Nature Portfolio
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spelling doaj-art-e617dd210bf84f3480d30c71577594ff2025-08-20T03:48:15ZengNature PortfolioNature Communications2041-17232025-05-0116111310.1038/s41467-025-59859-zOxytocinergic input from the paraventricular nucleus to the nucleus accumbens core modulates methamphetamine-conditioned place preferenceYing-jie Cheng0Gui-ying Zan1Ying-zhi Deng2Di Deng3Man-qing Wu4Jing-rui Chai5Yu-jun Wang6Jing-gen Liu7Min Zhao8Shanghai Mental Health Center, Shanghai Jiao Tong University School of MedicineKey Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of SciencesShanghai Mental Health Center, Shanghai Jiao Tong University School of MedicineShanghai Mental Health Center, Shanghai Jiao Tong University School of MedicineShanghai Mental Health Center, Shanghai Jiao Tong University School of MedicineKey Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of SciencesKey Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of SciencesKey Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of SciencesShanghai Mental Health Center, Shanghai Jiao Tong University School of MedicineAbstract Methamphetamine (METH) is a highly addictive psychostimulant, yet its addiction mechanisms remain unclear. Oxytocin (OXT), a neuropeptide, shows promise in reducing METH addiction, but how OXT exerts its effects is poorly understood. Using conditioned place preference (CPP), we first found that intranasal OXT other than Arginine Vasopressin (AVP) administration suppressed METH-CPP in mice, which could be reversed by OXT receptors (OXTRs) blockade in the nucleus accumbens (NAc) core. Activating OXTRs in the NAc core similarly reduced METH-CPP. Then, we found repeated METH exposure inhibited oxytocinergic neurons within the paraventricular nucleus (PVN) and lowered PVN OXT protein level. Chemogenetic activation of PVN oxytocinergic neurons (PVNOXT) blocked METH-CPP. Furthermore, METH inhibited PVNOXT-NAc core circuit other than PVNOXT-NAc shell circuit. Activation of PVNOXT-NAc core circuit significantly inhibited METH-CPP. This study reveals METH may impair the endogenous OXT system, especially the PVNOXT-NAc core circuit, highlighting OXT’s therapeutic potential for METH use disorder (MUD).https://doi.org/10.1038/s41467-025-59859-z
spellingShingle Ying-jie Cheng
Gui-ying Zan
Ying-zhi Deng
Di Deng
Man-qing Wu
Jing-rui Chai
Yu-jun Wang
Jing-gen Liu
Min Zhao
Oxytocinergic input from the paraventricular nucleus to the nucleus accumbens core modulates methamphetamine-conditioned place preference
Nature Communications
title Oxytocinergic input from the paraventricular nucleus to the nucleus accumbens core modulates methamphetamine-conditioned place preference
title_full Oxytocinergic input from the paraventricular nucleus to the nucleus accumbens core modulates methamphetamine-conditioned place preference
title_fullStr Oxytocinergic input from the paraventricular nucleus to the nucleus accumbens core modulates methamphetamine-conditioned place preference
title_full_unstemmed Oxytocinergic input from the paraventricular nucleus to the nucleus accumbens core modulates methamphetamine-conditioned place preference
title_short Oxytocinergic input from the paraventricular nucleus to the nucleus accumbens core modulates methamphetamine-conditioned place preference
title_sort oxytocinergic input from the paraventricular nucleus to the nucleus accumbens core modulates methamphetamine conditioned place preference
url https://doi.org/10.1038/s41467-025-59859-z
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