BEHAVIORAL ABNORMALITIES IN MALE-MICE LACKING NEURONAL NITRIC-OXIDE SYNTHASE

BEHAVIORAL ABNORMALITIES IN MALE-MICE LACKING NEURONAL NITRIC-OXIDE SYNTHASE
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DOI:
10.1038/378383a0
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发表时间:
1995-11-23
期刊:
影响因子:
64.8
通讯作者:
SNYDER, SH
SNYDER, SH
中科院分区:
综合性期刊1区
文献类型:
--
作者:
NELSON, RJ;DEMAS, GE;SNYDER, SH

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一氧化氮 (NO) 除了在血管 (1,2) 和巨噬细胞 (3,4) 功能中发挥作用外,它还是一种在情绪调节大脑区域 (6-8) 中高密度存在的神经递质 (5)。神经元一氧化氮合酶 (nNOS) 被靶向破坏的小鼠表现出大致正常的外观、运动活动、繁殖 (9)、长期增强和长期抑制 (11)。 nNOS(-) 小鼠对大脑中动脉结扎后的神经中风损伤具有抵抗力(12)。虽然野生型小鼠中 CO2 诱导的脑血管舒张是 NO 依赖性的,但在 nNOS(-) 小鼠中,这种血管舒张不受 NOS 抑制剂的影响 (13)。到目前为止,建立 NO 的行为作用还不可行,因为 NOS 抑制剂药物只能急性给药,而且它们对血压和其他身体功能的显着影响混淆了行为解释。我们现在报告 nNOS(-) 小鼠的攻击性行为和过度、不适当的性行为大量增加。
Is addition to its role in blood vessel(1,2) and macrophage(3,4) function, nitric oxide (NO) is a neurotransmitter(5) found in high densities in emotion-regulating brain regions(6-8). Mice with targeted disruption of neuronal NO synthase (nNOS) display grossly normal appearance, locomotor activity, breeding(9), long-term potentiation and long-term depression(11). The nNOS(-) mice are resistant to neural stroke damage following middle cerebral artery ligation(12). Although CO2-induced cerebral vasodilatation in wild-type mice is NO-dependent, in nNOS(-) mice this vasodilation is unaffected by NOS inhibitors(13). Establishing a behavioural role for NO has, until now, not been feasible, as NOS inhibitor drugs can only be administered acutely and because their pronounced effects on blood pressure and other body functions obfuscate behavioural interpretations. We now report a large increase in aggressive behaviour and excess, inappropriate sexual behaviour in nNOS(-) mice.