Gordon F J
Am J Physiol. 1987 Mar;252(3 Pt 2):R628-33. doi: 10.1152/ajpregu.1987.252.3.R628.
The purpose of this study was to identify central nervous system pathways and synaptic receptors that participate in baroreflex control of arterial pressure. Microinjections of excitatory amino acids into the caudal ventrolateral medulla (CVM) of anesthetized rats evoked depressor responses analogous to baroreceptor reflexes. Functional inactivation of CVM neurons produced by microinjection of the gamma-aminobutyric acid receptor agonist muscimol completely abolished baroreflex-mediated decreases in arterial pressure elicited by electrical stimulation of the aortic nerve and markedly reduced depressor responses produced by the excitatory amino acid L-glutamate. In contrast, selective blockade of N-methyl-D-aspartic acid (NMDA) receptors in the CVM abolished synaptically mediated depressor responses evoked by aortic nerve stimulation but not those elicited by L-glutamate, kainic acid, or quisqualic acid injected at the same site. These results indicate that the CVM contains an obligatory synapse in the central aortic baroreflex pathway; neural transmission of aortic baroreceptor information in the CVM is mediated by activation of NMDA receptors; and the neurotransmitter released at CVM synapses may be an excitatory amino acid.
本研究的目的是确定参与动脉压力压力感受性反射控制的中枢神经系统通路和突触受体。向麻醉大鼠的尾侧腹外侧延髓（CVM）微量注射兴奋性氨基酸可诱发类似于压力感受器反射的降压反应。通过微量注射γ-氨基丁酸受体激动剂蝇蕈醇使CVM神经元功能失活，完全消除了电刺激主动脉神经引起的压力感受性反射介导的动脉血压下降，并显著降低了兴奋性氨基酸L-谷氨酸引起的降压反应。相比之下，选择性阻断CVM中的N-甲基-D-天冬氨酸（NMDA）受体可消除主动脉神经刺激诱发的突触介导的降压反应，但不能消除在同一部位注射L-谷氨酸、 kainic酸或quisqualic酸所诱发的降压反应。这些结果表明，CVM在中枢主动脉压力感受性反射通路中包含一个必需的突触；CVM中主动脉压力感受器信息的神经传递是由NMDA受体的激活介导的；并且在CVM突触处释放的神经递质可能是一种兴奋性氨基酸。
