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首页> 外文期刊>Behavioural Brain Research: An International Journal >Role of ventral hippocampal nitric oxide/cGMP pathway in anxiety-related behaviors in rats submitted to the elevated T-maze.
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Role of ventral hippocampal nitric oxide/cGMP pathway in anxiety-related behaviors in rats submitted to the elevated T-maze.

机译:腹侧海马一氧化氮/ cGMP通路在T型迷宫抬高的大鼠焦虑相关行为中的作用。

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摘要

The L-arginineitric oxide (NO)/cGMP pathways have been implicated in the control of a variety of physiological mechanisms and are believed to participate in the modulation of anxiety in the CNS. The aim of this study was to investigate the effects of N(G)-nitro-L-arginine-methyl-ester (L-NAME), a non-selective inhibitor of NO synthase (NOS); 7-nitroindazole (7-NI), a preferential inhibitor of neuronal NOS; and sodium nitroprusside (SNP), an NO donor, administered into the ventral hippocampus (VH) of rats submitted to the elevated T-maze (ETM). The ETM, an animal model derived from the elevated plus-maze, allows the measurement of two defensive behavioral responses in the same rat: inhibitory avoidance and escape. Results showed that L-NAME and 7-NI impaired the acquisition of inhibitory avoidance and prolonged escape latency in the ETM, suggesting an anxiolytic-like and panicolytic-like effect, respectively. SNP facilitated the acquisition of inhibitory avoidance without interfering with escape performance, suggesting an anxiogenic-like effect. Treatment with methylene blue did not alter per se any of the behavioral responses measured in the ETM, but blocked the effect promoted by SNP. Thus, altogether these results suggest that NO in the VH is critically involved in the modulation of defensive behavior of rats exposed to the ETM.
机译:L-精氨酸/一氧化氮(NO)/ cGMP途径已牵涉到各种生理机制的控制,并被认为参与中枢神经系统中焦虑的调节。这项研究的目的是研究N(G)-硝基-L-精氨酸甲酯(L-NAME)的作用,N-G是一种非选择性的NO合酶抑制剂。 7-硝基吲唑(7-NI),神经元NOS的优先抑制剂;硝普钠(NO)的硝普钠(SNP)被施用于呈高架T型迷宫(ETM)的大鼠腹侧海马(VH)。 ETM是一种从高架迷宫产生的动物模型,可以测量同一只大鼠的两种防御行为反应:抑制回避和逃避。结果表明,L-NAME和7-NI削弱了ETM中抑制性规避的获得和延长的逃逸潜伏期,分别表明了抗焦虑药和panicolytic药的作用。 SNP有助于获得抑制性回避,而不会干扰逃逸性能,表明有类似焦虑的作用。亚甲基蓝处理本身并不会改变ETM中测得的任何行为反应,但会阻止SNP促进的作用。因此,总而言之,这些结果表明,VH中的NO关键参与了暴露于ETM的大鼠的防御行为的调节。

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