GluA3-deficiency in mice is associated with increased social and aggressive behavior and elevated dopamine in striatum.
GluA3-deficiency in mice is associated with increased social and aggressive behavior and elevated dopamine in striatum.
复制标题
DOI：
10.1016/j.bbr.2012.01.007
复制
发表时间：
2012-04-01
影响因子：
2.7
通讯作者：
Wang, Tao
中科院分区：
文献类型：
--
作者：
Adamczyk, Abby;Mejias, Rebeca;Takamiya, Kogo;Yocum, Jennifer;Krasnova, Irina N.;Calderon, Juan;Cadet, Jean Lud;Huganir, Richard L.;Pletnikov, Mikhail V.;Wang, Tao
关键词：
Glutamate signaling has been implicated in the regulation of social behavior. AMPA-glutamate receptors are assembled from four subunits (GluA1-4) of mainly GluA1/2 and GluA2/3 tetramers that form ion channels of distinct functional properties. Mice lacking GluA1 showed a reduced anxiety and male aggression. To understand the role of GluA3 in modulating social behavior, we investigated GluA3-deficient mice (Gria3 -/Y) on C57BL/6J background. Compared to wild type (WT) littermates (n=14), Gria3 -/Y mice (n=13) showed an increase in isolation-induced male aggression (p=0.011) in home cage resident-intruder test; an increase in sociality (p=0.01), and increase in male-male social interactions in neutral arena (p=0.005); an increase in peripheral activities in open field test (p=0.037) with normal anxiety levels in elevated plus maze and light-dark box; and minor deficits in motor and balance function in accelerating rotarod test (p=0.016) with normal grip strength. Gria3 -/Y mice showed no significant deficit in spatial memory function in Morris-water maze and Y-maze tests, and normal levels of testosterone. Increased dopamine concentrations in stratum (p=0.034) and reduced serotonin turnover in olfactory bulb (p=0.002) were documented in Gria3 -/Y mice. These results support a role of GluA3 in the modulation of social behavior through brain dopamine and/or serotonin signaling and different AMPA receptor subunits affect social behavior through distinct mechanisms.
登录
查看更多内容
影响因子：
2.9
作者：
Deng, Yun-Ping;Shelby, Evan;Reiner, Anton J.
通讯作者：
Reiner, Anton J.
影响因子：
2.9
作者：
Garris, DR
通讯作者：
Garris, DR
影响因子：
3.6
作者：
Kudryavtseva, NN;Lipina, TV;Koryakina, LA
通讯作者：
Koryakina, LA
影响因子：
16.2
作者：
Mansour, M;Nagarajan, N;Rosenmund, C
通讯作者：
Rosenmund, C
影响因子：
16.2
作者：
Ayalon, G;Stern-Bach, Y
通讯作者：
Stern-Bach, Y