Glutamic acid decarboxylase (GAD65) immunoreactivity in brains of aggressive, adolescent anabolic steroid-treated hamsters

Glutamic acid decarboxylase (GAD65) immunoreactivity in brains of aggressive, adolescent anabolic steroid-treated hamsters
复制标题

DOI:
10.1016/s0018-506x(03)00138-7
复制
发表时间:
2003-09-01
影响因子:
3.5
通讯作者:
Melloni, RH
Melloni, RH
中科院分区:
医学3区
文献类型:
--
作者:
Grimes, JM;Ricci, LA;Melloni, RH

文献摘要

被引文献

相似文献

慢性同化雄激素(AAS)治疗青春期促进进攻性攻击雄性叙利亚仓鼠(Mesocricetus auratus)。目前的研究评估了青少年AAS暴露是否影响谷氨酸脱羧酶(GAD(65))的免疫组织化学定位,谷氨酸脱羧酶是γ-氨基丁酸(GABA)合成的限速酶,在仓鼠大脑中涉及攻击行为的区域。在整个青春期对仓鼠给予高剂量AAS,对攻击性攻击进行评分,然后检查GAD(65)斑点与仓鼠大脑中对攻击性重要的区域的差异。与对照组相比,攻击性AAS处理的仓鼠在几个攻击性区域(包括前下丘脑、腹外侧下丘脑和内侧杏仁核)的GAD(65)免疫反应斑点所覆盖的面积显著增加。相反,与油处理的对照组相比,攻击性AAS处理的仓鼠显示侧隔中GA(65)-ir斑点显著减少。而在终纹床核和中央杏仁核等其他攻击区,GAD(65)点的表达无显著差异。总之,这些结果支持改变GAD(65)的合成和功能在青少年AAS促进攻击性攻击的作用。(C)2003年爱思唯尔公司All rights reserved.
Chronic anabolic-androgenic steroid (AAS) treatment during adolescence facilitates offensive aggression in male Syrian hamsters (Mesocricetus auratus). The current study assessed whether adolescent AAS exposure influenced the immunohistochemical localization of glutamic acid decarboxylase (GAD(65)), the rate-limiting enzyme in the synthesis of gamma-aminobutyric acid (GABA), in areas of hamster brain implicated in aggressive behavior. Hamsters were administered high dose AAS throughout adolescence, scored for offensive aggression, and then examined for differences in GAD(65) puncta to regions of the hamster brain important for aggression. When compared with control animals, aggressive AAS-treated hamsters showed significant increases in the area covered by GAD(65) immunoreactive puncta in several of these aggression regions, including the anterior hypothalamus, ventrolateral hypothalamus, and medial amygdala. Conversely, aggressive AAS-treated hamsters showed a significant decrease in GA(65)-ir puncta in the lateral septum when compared with oil-treated controls. However, no differences in GAD(65) puncta were found in other aggression areas, such as the bed nucleus of the stria terminalis and central amygdala. Together, these results support a role for altered GAD(65) synthesis and function in adolescent AAS-facilitated offensive aggression. (C) 2003 Elsevier Inc. All rights reserved.