Loss of GluN2D subunit results in social recognition deficit, social stress, 5-HT 2C receptor dysfunction, and anhedonia in mice
作者: Hideko YamamotoEtsuko KamegayaYoko HaginoYukio TakamatsuWakako SawadaMaaya MatsuzawaSoichiro IdeToshifumi YamamotoMasayoshi MishinaKazutaka Ikeda
作者单位: 1Addictive Substance Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan
2Laboratory of Molecular Psychopharmacology, Graduate School of Nanosciences, Yokohama City University, Yokohama 236-0027, Japan
3Ritsumeikan University Research Organization of Science and Technology, Kusatsu 525-8577, Japan
刊名: Neuropharmacology, 2017, Vol.112 , pp.188-197
来源数据库: Elsevier Journal
DOI: 10.1016/j.neuropharm.2016.07.036
关键词: GluN2D subunitBehaviorAnhedoniaDepressionDeficit in social recognitionGolgi-Cox staining5-Hydroxytryptamine-2C
英文摘要: Abstract(#br)The N -methyl- d -aspartate (NMDA) receptor channel is involved in various physiological functions, including learning and memory. The GluN2D subunit of the NMDA receptor has low expression in the mature brain, and its role is not fully understood. In the present study, the effects of GluN2D subunit deficiency on emotional and cognitive function were investigated in GluN2D knockout (KO) mice. We found a reduction of motility (i.e., a depressive-like state) in the tail suspension test and a reduction of sucrose preference (i.e., an anhedonic state) in GluN2D KO mice that were group-housed with littermates. Despite apparently normal olfactory function and social interaction, GluN2D KO mice exhibited a decrease in preference for social novelty, suggesting a deficit in social...
全文获取路径: Elsevier  (合作)
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影响因子:4.114 (2012)

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