@article{ref1,
title="GluA3-deficiency in mice is associated with increased social and aggressive behavior and elevated dopamine in striatum",
journal="Behavioural brain research",
year="2012",
author="Adamczyk, Abby and Mejias, Rebeca and Takamiya, Kogo and Yocum, Jennifer and Krasnova, Irina and Calderon, Juan and Cadet, Jean Lud and Huganir, Richard and Pletnikov, Mikhail and Wang, Tao",
volume="229",
number="1",
pages="265-272",
abstract="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.<p /> <p>Language: en</p>",
language="en",
issn="0166-4328",
doi="10.1016/j.bbr.2012.01.007",
url="http://dx.doi.org/10.1016/j.bbr.2012.01.007"
}