Loss of GluN2D subunit results in social recognition deficit, social stress, 5-HT_2C receptor dysfunction, and anhedonia in mice

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• 作者：Hideko Yamamoto^a ; ^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 Kamegaya^a ; Yoko Hagino^a ; Yukio Takamatsu^a ; Wakako Sawada^a ; Maaya Matsuzawa^a ; ^b ; Soichiro Ide^a ; Toshifumi Yamamoto^a ; ^b ; Masayoshi Mishina^c ; Kazutaka Ikeda^a
• 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

<dl class="listitem" id="list_ulist0010"><dt class="label">•dt><dd>

d="p0010">The GluN2D subunit ablation impaired social recognition but not object recognition.

dd><dt class="label">•dt><dd>

d="p0015">Impaired social recognition caused social stress, anhedonic- and depressive states.

dd><dt class="label">•dt><dd>

d="p0020">5-HT_2C receptor antagonism improved these anhedonic- and depressive-like states.

dd><dt class="label">•dt><dd>

d="p0025">GluN2D KO mice may be a useful animal model of chronic social stress.

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