Loss of GluN2D subunit results in social recognition deficit, social stress, 5-HT2C receptor dysfunction, and anhedonia in mice
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- 作者：Hideko Yamamotoa ; b ; yamamoto-hd@igakuken.or.jp" class="auth_mail" title="E-mail the corresponding author ; yamahide@yokohama-cu.ac.jp" class="auth_mail" title="E-mail the corresponding author ; Etsuko Kamegayaa ; Yoko Haginoa ; Yukio Takamatsua ; Wakako Sawadaa ; Maaya Matsuzawaa ; b ; Soichiro Idea ; Toshifumi Yamamotoa ; b ; Masayoshi Mishinac ; Kazutaka Ikedaa
- 关键词：GluN2D subunit ; Behavior ; Anhedonia ; Depression ; Deficit in social recognition ; Golgi-Cox staining ; 5-Hydroxytryptamine-2C
- 刊名：Neuropharmacology
- 出版年：2017
- 出版时间：January 2017
- 年：2017
- 卷：112
- 期：part_PA
- 页码：188-197
- 全文大小：2763 K
文摘
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The GluN2D subunit ablation impaired social recognition but not object recognition.
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Impaired social recognition caused social stress, anhedonic- and depressive states.
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5-HT2C receptor antagonism improved these anhedonic- and depressive-like states.
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GluN2D KO mice may be a useful animal model of chronic social stress.
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