« Previous AbstractInsect pheromone behavior: fruit fly    Next AbstractApproaches to insect control based on chemical ecology--case studies »

Neuropharmacology

Title:		"Loss of GluN2D subunit results in social recognition deficit, social stress, 5-HT(2C) receptor dysfunction, and anhedonia in mice"
Author(s):		Yamamoto H; Kamegaya E; Hagino Y; Takamatsu Y; Sawada W; Matsuzawa M; Ide S; Yamamoto T; Mishina M; Ikeda K;
Address:		"Addictive Substance Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan; Laboratory of Molecular Psychopharmacology, Graduate School of Nanosciences, Yokohama City University, Yokohama 236-0027, Japan. Electronic address: yamamoto-hd@igakuken.or.jp. Addictive Substance Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan. Addictive Substance Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan; Laboratory of Molecular Psychopharmacology, Graduate School of Nanosciences, Yokohama City University, Yokohama 236-0027, Japan. Ritsumeikan University Research Organization of Science and Technology, Kusatsu 525-8577, Japan"
Journal Title:		Neuropharmacology
Year:		2017
Volume:		20160730
Issue:		Pt A
Page Number:		188 - 197
DOI:		10.1016/j.neuropharm.2016.07.036
ISSN/ISBN:		1873-7064 (Electronic) 0028-3908 (Linking)
Abstract:		"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 recognition or memory. Golgi-Cox staining revealed a reduction of the complexity of dendritic trees in the accessory olfactory bulb in GluN2D KO mice, suggesting a deficit in pheromone processing pathway activation, which modulates social recognition. The deficit in social recognition may result in social stress in GluN2D KO mice. Isolation housing is a procedure that has been shown to reduce stress in mice. Interestingly, 3-week isolation and treatment with agomelatine or the 5-hydroxytryptamine-2C (5-HT(2C)) receptor antagonist SB242084 reversed the anhedonic-like state in GluN2D KO mice. In contrast, treatment with the 5-HT(2C) receptor agonist CP809101 induced depressive- and anhedonic-like states in isolated GluN2D KO mice. These results suggest that social stress that is caused by a deficit in social recognition desensitizes 5-HT(2c) receptors, followed by an anhedonic- and depressive-like state, in GluN2D KO mice. The GluN2D subunit of the NMDA receptor appears to be important for the recognition of individuals and development of normal emotionality in mice. 5-HT(2C) receptor antagonism may be a therapeutic target for treating social stress-induced anhedonia. This article is part of the Special Issue entitled 'Ionotropic glutamate receptors'"
Keywords:		"Acetamides/pharmacology Aminopyridines/pharmacology Anhedonia/*physiology Animals Dendrites/pathology Indoles/pharmacology Mice Mice, Knockout Olfactory Bulb/pathology Protein Subunits/genetics/physiology Receptor, Serotonin, 5-HT2C/*physiology Receptors, ;"
Notes:		"MedlineYamamoto, Hideko Kamegaya, Etsuko Hagino, Yoko Takamatsu, Yukio Sawada, Wakako Matsuzawa, Maaya Ide, Soichiro Yamamoto, Toshifumi Mishina, Masayoshi Ikeda, Kazutaka eng England 2016/10/25 Neuropharmacology. 2017 Jan; 112(Pt A):188-197. doi: 10.1016/j.neuropharm.2016.07.036. Epub 2016 Jul 30"