CREB regulation of nucleus accumbens excitability mediates social isolation–induced behavioral deficits

被引:0
|
作者
Deanna L Wallace
Ming-Hu Han
Danielle L Graham
Thomas A Green
Vincent Vialou
Sergio D Iñiguez
Jun-Li Cao
Anne Kirk
Sumana Chakravarty
Arvind Kumar
Vaishnav Krishnan
Rachael L Neve
Don C Cooper
Carlos A Bolaños
Michel Barrot
Colleen A McClung
Eric J Nestler
机构
[1] University of Texas Southwestern Medical Center,Departments of Psychiatry and Neuroscience
[2] 5323 Harry Hines Boulevard,Fishberg Department of Neuroscience
[3] Mount Sinai School of Medicine,Department of Psychology
[4] One Gustav L. Levy Place Box 1065,Department of Psychiatry
[5] Florida State University,undefined
[6] Harvard Medical School,undefined
[7] McLean Hospital,undefined
[8] Institut des Neurosciences Cellulaires et Intégratives,undefined
[9] UMR7168,undefined
[10] CNRS and University Louis Pasteur,undefined
[11] 21 Rue Descartes,undefined
[12] Present addresses: Helen Willis Neuroscience Institute,undefined
[13] University of California Berkeley,undefined
[14] 132 Barker Hall,undefined
[15] Berkeley,undefined
[16] California 94720,undefined
[17] USA (D.L.W.),undefined
[18] Merck Laboratories,undefined
[19] 33 Avenue Louis Pasteur,undefined
[20] Boston,undefined
[21] Massachusetts 02115,undefined
[22] USA (D.L.G.),undefined
[23] and Department of Pharmacology and Toxicology,undefined
[24] Virginia Commonwealth University,undefined
[25] 1112 East Clay Street,undefined
[26] Richmond,undefined
[27] Virginia 23298,undefined
[28] USA (T.A.G.).,undefined
来源
Nature Neuroscience | 2009年 / 12卷
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摘要
cAMP response element–binding protein (CREB) is a key regulator of the nucleus accumbens shell function in animals' responses to emotional stimuli. The present study demonstrates that passive stress in the form of social isolation induces anhedonia and depression-like symptoms that are mediated by CREB activity and neuronal excitability.
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页码:200 / 209
页数:9
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