Urbanski R W, Sapru H N
Department of Pharmacology, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark 07103.
J Auton Nerv Syst. 1988 Aug;23(2):161-74. doi: 10.1016/0165-1838(88)90080-x.
The role of the ventrolateral medullary pressor (VLPA) and depressor (VLDA) areas in mediating cardiovascular responses evoked from the nucleus tractus solitarius (NTS) was investigated. Male Wistar rats, anesthetized with pentobarbital or urethane, were artificially ventilated and blood pressure (BP) and heart rate (HR) were monitored. The VLPA, VLDA, and the NTS were identified bilaterally with microinjections of L-glutamate. Unilateral microinjections of muscimol or lidocaine into the VLPA or the VLDA blocked the decrease in BP produced by microinjections of L-glutamate (1.77 nmol) into the NTS. These findings indicate that both areas are essential for mediating depressor responses elicited from the NTS. When neuronal activity in the VLDA was depressed unilaterally (leaving the ipsilateral VLPA intact), with the microinjection of muscimol or lidocaine, microinjection of a larger dose (5.0 nmol) of L-glutamate into the ipsilateral NTS elicited a pressor response. This response was blocked by depressing neuronal activity in the ipsilateral VLPA by microinjection of muscimol into this site. This pressor response evoked from the NTS was not due to non-specific effects of L-glutamate since repeated microinjections of L-glutamate (5.0 nmol/site) into the NTS consistently produced decreases in BP and HR. The stimulation of the contralateral NTS by glutamate continued to elicit the usual decreases in BP and HR. Microinjections of either dose (1.77 or 5 nmol) of L-glutamate into the areas adjacent to the NTS (e.g. 1.0 mm rostral or lateral to the NTS, the gracile or cuneate nuclei and area postrema) failed to evoke any cardiovascular responses indicating that the responses were mediated by neurons localized within the intermediate one-third of the NTS. These results indicate that: (1) the depressor responses elicited from the NTS involve the pathways from the NTS to the VLDA and VLDA to VLPA and (2) there may be a pathway from the NTS to the VLPA which is sympathoexcitatory and is unmasked when neuronal activity in the VLDA is depressed.
研究了延髓腹外侧加压区（VLPA）和减压区（VLDA）在介导孤束核（NTS）诱发的心血管反应中的作用。用戊巴比妥或乌拉坦麻醉的雄性Wistar大鼠进行人工通气，并监测血压（BP）和心率（HR）。通过微量注射L-谷氨酸对双侧的VLPA、VLDA和NTS进行定位。向VLPA或VLDA单侧微量注射蝇蕈醇或利多卡因可阻断向NTS微量注射L-谷氨酸（1.77 nmol）所产生的血压下降。这些发现表明，这两个区域对于介导NTS诱发的减压反应至关重要。当通过微量注射蝇蕈醇或利多卡因单侧抑制VLDA中的神经元活动（同侧VLPA保持完整）时，向同侧NTS微量注射更大剂量（5.0 nmol）的L-谷氨酸会引发加压反应。通过向该部位微量注射蝇蕈醇抑制同侧VLPA中的神经元活动可阻断该反应。从NTS诱发的这种加压反应并非由于L-谷氨酸的非特异性作用，因为向NTS重复微量注射L-谷氨酸（5.0 nmol/部位）始终会导致血压和心率下降。谷氨酸对侧NTS的刺激继续引发通常的血压和心率下降。向NTS相邻区域（例如NTS头端或外侧1.0 mm处、薄束核或楔束核以及最后区）微量注射任一剂量（1.77或5 nmol）的L-谷氨酸均未引发任何心血管反应，这表明这些反应是由位于NTS中间三分之一区域内的神经元介导的。这些结果表明：（1）从NTS诱发的减压反应涉及从NTS到VLDA以及从VLDA到VLPA的通路；（2）可能存在一条从NTS到VLPA的通路，该通路具有交感兴奋作用，并且在VLDA中的神经元活动受到抑制时会被揭示出来。
