AMPK signaling in the nucleus accumbens core mediates cue-induced reinstatement of cocaine seeking

Abstract Relapse to drug seeking can be caused by exposure to drug-associated cues, provoking drug craving even after prolonged abstinence. Recent studies demonstrated that AMP-activated protein kinase (AMPK) regulates neuronal morphology and membrane excitability in neurons. Here, we investigated t...

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Autores principales:	Xue-Jiao Gao, Kai Yuan, Lu Cao, Wei Yan, Yi-Xiao Luo, Min Jian, Jian-Feng Liu, Qin Fang, Ji-Shi Wang, Ying Han, Jie Shi, Lin Lu
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/d2f58ef33d144a0cbaf64dd15bcb6255
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spelling	oai:doaj.org-article:d2f58ef33d144a0cbaf64dd15bcb62552021-12-02T11:40:50ZAMPK signaling in the nucleus accumbens core mediates cue-induced reinstatement of cocaine seeking10.1038/s41598-017-01043-52045-2322https://doaj.org/article/d2f58ef33d144a0cbaf64dd15bcb62552017-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-01043-5https://doaj.org/toc/2045-2322Abstract Relapse to drug seeking can be caused by exposure to drug-associated cues, provoking drug craving even after prolonged abstinence. Recent studies demonstrated that AMP-activated protein kinase (AMPK) regulates neuronal morphology and membrane excitability in neurons. Here, we investigated the role of AMPK activity in the nucleus accumbens (NAc) in relapse to cocaine seeking. We found that exposure to drug-related cues reinstated cocaine-seeking behavior and increased AMPK and p70s6k phosphorylation in the NAc core but not shell. Augmenting AMPK activity by intra-NAc core infusions of the AMPK activator 5-amino-1-β-D-ribofuranosyl-imidazole-4-carboxamide (AICAR) or adenovirus expressing constitutively active subunits of AMPK decreased cue-induced reinstatement of cocaine seeking and inhibited the mammalian target of rapamycin complex 1 (mTORC1) and extracellular signal-regulated kinase 1/2 (ERK1/2) pathways. In contrast, inhibition of AMPK activity by intra-NAc core infusions of the AMPK inhibitor compound C or adenovirus expressing dominant-negative subunits of AMPK increased cue-induced reinstatement of cocaine seeking and enhanced mTORC1 and ERK1/2 activity. The regulation of AMPK activity in the NAc shell had no effect on cue-induced cocaine seeking. Altogether, these results indicate that AMPK activity in the NAc core is critical for the cue-induced reinstatement of cocaine seeking, which may be mediated by mTORC1 and ERK1/2 signaling.Xue-Jiao GaoKai YuanLu CaoWei YanYi-Xiao LuoMin JianJian-Feng LiuQin FangJi-Shi WangYing HanJie ShiLin LuNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Xue-Jiao Gao Kai Yuan Lu Cao Wei Yan Yi-Xiao Luo Min Jian Jian-Feng Liu Qin Fang Ji-Shi Wang Ying Han Jie Shi Lin Lu AMPK signaling in the nucleus accumbens core mediates cue-induced reinstatement of cocaine seeking
description	Abstract Relapse to drug seeking can be caused by exposure to drug-associated cues, provoking drug craving even after prolonged abstinence. Recent studies demonstrated that AMP-activated protein kinase (AMPK) regulates neuronal morphology and membrane excitability in neurons. Here, we investigated the role of AMPK activity in the nucleus accumbens (NAc) in relapse to cocaine seeking. We found that exposure to drug-related cues reinstated cocaine-seeking behavior and increased AMPK and p70s6k phosphorylation in the NAc core but not shell. Augmenting AMPK activity by intra-NAc core infusions of the AMPK activator 5-amino-1-β-D-ribofuranosyl-imidazole-4-carboxamide (AICAR) or adenovirus expressing constitutively active subunits of AMPK decreased cue-induced reinstatement of cocaine seeking and inhibited the mammalian target of rapamycin complex 1 (mTORC1) and extracellular signal-regulated kinase 1/2 (ERK1/2) pathways. In contrast, inhibition of AMPK activity by intra-NAc core infusions of the AMPK inhibitor compound C or adenovirus expressing dominant-negative subunits of AMPK increased cue-induced reinstatement of cocaine seeking and enhanced mTORC1 and ERK1/2 activity. The regulation of AMPK activity in the NAc shell had no effect on cue-induced cocaine seeking. Altogether, these results indicate that AMPK activity in the NAc core is critical for the cue-induced reinstatement of cocaine seeking, which may be mediated by mTORC1 and ERK1/2 signaling.
format	article
author	Xue-Jiao Gao Kai Yuan Lu Cao Wei Yan Yi-Xiao Luo Min Jian Jian-Feng Liu Qin Fang Ji-Shi Wang Ying Han Jie Shi Lin Lu
author_facet	Xue-Jiao Gao Kai Yuan Lu Cao Wei Yan Yi-Xiao Luo Min Jian Jian-Feng Liu Qin Fang Ji-Shi Wang Ying Han Jie Shi Lin Lu
author_sort	Xue-Jiao Gao
title	AMPK signaling in the nucleus accumbens core mediates cue-induced reinstatement of cocaine seeking
title_short	AMPK signaling in the nucleus accumbens core mediates cue-induced reinstatement of cocaine seeking
title_full	AMPK signaling in the nucleus accumbens core mediates cue-induced reinstatement of cocaine seeking
title_fullStr	AMPK signaling in the nucleus accumbens core mediates cue-induced reinstatement of cocaine seeking
title_full_unstemmed	AMPK signaling in the nucleus accumbens core mediates cue-induced reinstatement of cocaine seeking
title_sort	ampk signaling in the nucleus accumbens core mediates cue-induced reinstatement of cocaine seeking
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/d2f58ef33d144a0cbaf64dd15bcb6255
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AMPK signaling in the nucleus accumbens core mediates cue-induced reinstatement of cocaine seeking

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