Cases O, Seif I, Grimsby J, Gaspar P, Chen K, Pournin S, Müller U, Aguet M, Babinet C, Shih J C
Centre National de la Recherche Scientifique (CNRS), Unité de Recherche Associée (URA), Institut Curie, Orsay, France.
Science. 1995 Jun 23;268(5218):1763-6. doi: 10.1126/science.7792602.
Deficiency in monoamine oxidase A (MAOA), an enzyme that degrades serotonin and norepinephrine, has recently been shown to be associated with aggressive behavior in men of a Dutch family. A line of transgenic mice was isolated in which transgene integration caused a deletion in the gene encoding MAOA, providing an animal model of MAOA deficiency. In pup brains, serotonin concentrations were increased up to ninefold, and serotonin-like immunoreactivity was present in catecholaminergic neurons. In pup and adult brains, norepinephrine concentrations were increased up to twofold, and cytoarchitectural changes were observed in the somatosensory cortex. Pup behavioral alterations, including trembling, difficulty in righting, and fearfulness were reversed by the serotonin synthesis inhibitor parachlorophenylalanine. Adults manifested a distinct behavioral syndrome, including enhanced aggression in males.
单胺氧化酶A(MAOA)是一种降解血清素和去甲肾上腺素的酶,最近研究表明,荷兰一个家族中的男性若缺乏该酶,则与攻击性行为有关。研究分离出了一组转基因小鼠,其中转基因整合导致编码MAOA的基因发生缺失,从而提供了一个MAOA缺乏的动物模型。在幼鼠大脑中,血清素浓度增加了九倍,并且在儿茶酚胺能神经元中存在血清素样免疫反应。在幼鼠和成年鼠大脑中,去甲肾上腺素浓度增加了两倍,并且在体感皮层观察到细胞结构变化。血清素合成抑制剂对氯苯丙氨酸可逆转幼鼠的行为改变,包括颤抖、翻正困难和恐惧。成年鼠表现出一种独特的行为综合征,包括雄性攻击性增强。