Activin receptor signaling regulates cocaine-primed behavioral and morphological plasticity

被引：44

作者：

Gancarz, Amy M. ^{[1
]}

Wang, Zi-Jun ^{[1
]}

Schroeder, Gabrielle L. ^{[1
]}

Damez-Werno, Diane ^{[2
]}

Braunscheidel, Kevin M. ^{[1
]}

Mueller, Lauren E. ^{[1
]}

Humby, Monica S. ^{[1
]}

Caccamise, Aaron ^{[1
]}

Martin, Jennifer A. ^{[1
]}

Dietz, Karen C. ^{[1
]}

Neve, Rachael L. ^{[3
]}

Dietz, David M. ^{[1
]}

机构：

[1] SUNY Buffalo, Program Neurosci, Res Inst Addict, Dept Pharmacol & Toxicol, Buffalo, NY 14260 USA

[2] Icahn Sch Med Mt Sinai, Dept Neurosci, New York, NY 10029 USA

[3] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA

来源：

NATURE NEUROSCIENCE | 2015年 / 18卷 / 07期

关键词：

GROWTH-FACTOR-BETA; NUCLEUS-ACCUMBENS NEURONS; PROLONGED WITHDRAWAL; SYNAPTIC PLASTICITY; PREFRONTAL CORTEX; RATS; INCUBATION; ADDICTION; BRAIN; SMAD3;

D O I：

10.1038/nn.4036

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Activin receptor signaling, including the transcription factor Smad3, was upregulated in the rat nucleus accumbens (NAc) shell following withdrawal from cocaine. Direct genetic and pharmacological manipulations of this pathway bidirectionally altered cocaine seeking while governing morphological plasticity in NAc neurons. Thus, Activin/Smad3 signaling is induced following withdrawal from cocaine, and such regulation may be a key molecular mechanism underlying behavioral and cellular plasticity in the brain following cocaine self-administration.

引用

页码：959 / +

页数：6

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