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N-甲基-D-天冬氨酸(NMDA)受体拮抗剂可阻断未麻醉大鼠孤束核(NTS)内微量注射L-谷氨酸引起的心动过缓反应,但不能阻断升压反应。

NMDA receptor antagonist blocks the bradycardic but not the pressor response to L-glutamate microinjected into the nucleus tractus solitarius (NTS) of unanesthetized rats.

作者信息

Colombari E, Bonagamba L G, Machado B H

机构信息

Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Brazil.

出版信息

Brain Res. 1997 Feb 28;749(2):209-13. doi: 10.1016/S0006-8993(96)01169-9.

Abstract

In the present study we evaluated the role of NMDA receptors on the pressor and bradycardic responses to L-glutamate (L-Glu) microinjected into the nucleus tractus solitarius (NTS) of unanesthetized rats. L-Glu (1 nmol/100 nl) was microinjected into the NTS before and 10 min after microinjection of phosponovaleric acid (AP-5), a selective NMDA receptor antagonist, into the NTS of three different groups of rats (0.5, 2.0 and 10.0 nmol/100 nl). Microinjection of AP-5 into the NTS produced a dose-dependent reduction in the bradycardic response to L-Glu. However, no significant change in the pressor response to L-Glu was observed. These results indicate that the activation of the cardiovagal component (bradycardia) by L-Glu involves NMDA receptors and suggest that the activation of the sympatho-excitatory component (pressor response) by L-Glu in the commissural NTS is mediated by non-NMDA receptors.

摘要

在本研究中,我们评估了N-甲基-D-天冬氨酸(NMDA)受体在未麻醉大鼠孤束核(NTS)中对微量注射L-谷氨酸(L-Glu)所产生的升压和心动过缓反应中的作用。在三组不同的大鼠(0.5、2.0和10.0 nmol/100 nl)的NTS中微量注射选择性NMDA受体拮抗剂磷酸戊二酸(AP-5)之前以及之后10分钟,将L-Glu(1 nmol/100 nl)微量注射到NTS中。向NTS中微量注射AP-5可使对L-Glu的心动过缓反应呈剂量依赖性降低。然而,未观察到对L-Glu的升压反应有显著变化。这些结果表明,L-Glu对心迷走神经成分(心动过缓)的激活涉及NMDA受体,并提示L-Glu在连合NTS中对交感兴奋成分(升压反应)的激活是由非NMDA受体介导的。

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