Nikolaus S, Huston J P, Hasenöhrl R U
Institute of Physiological Psychology, University of Düsseldorf, Germany.
Neuroreport. 1999 Aug 2;10(11):2293-6. doi: 10.1097/00001756-199908020-00013.
We reported previously that the neurokinin substance P has anxiolytic-like effects when administered into the nucleus basalis of the rat ventral pallidum. The present study aimed to determine the possible involvement of the neurokinin-1 receptor in the anxiolytic action of intrabasalis substance P injection. Behavioral testing was performed in the rat elevated plus-maze model of anxiety. Microinjection of substance P (1 ng) into the nucleus basalis increased sojourn times on the open arms, excursions into the end of the open arms and scanning over the edge of an open arm, indicative of an anxiolytic-like profile. The non-peptide neurokinin-1 receptor antagonist WIN51,708, administered i.p. 20 min prior to intrabasalis substance P injection, antagonized the anxiolytic effects of the neurokinin in a dose-dependent manner. WIN51,708 at 10 mg/kg diminished, while at the higher dose of 20 mg/kg the antagonist completely blocked, the effect of substance P on anxiety-related behaviors. These findings suggest that the anxiolytic-like effects of substance P in the nucleus basalis are mediated through neurokinin-1 receptive sites.
我们之前报道过，当将神经激肽P物质注入大鼠腹侧苍白球基底核时，它具有类似抗焦虑的作用。本研究旨在确定神经激肽1受体是否可能参与基底核内注射P物质的抗焦虑作用。在大鼠高架十字迷宫焦虑模型中进行行为测试。向基底核微量注射P物质（1纳克）可增加在开放臂上的停留时间、进入开放臂末端的次数以及在开放臂边缘的扫视次数，这表明具有类似抗焦虑的表现。在基底核内注射P物质前20分钟腹腔注射非肽类神经激肽1受体拮抗剂WIN51,708，以剂量依赖的方式拮抗神经激肽的抗焦虑作用。10毫克/千克的WIN51,708可减弱，而在20毫克/千克的较高剂量时，该拮抗剂可完全阻断P物质对焦虑相关行为的作用。这些发现表明，基底核中P物质的类似抗焦虑作用是通过神经激肽1受体位点介导的。
