Agarwal S K, Gelsema A J, Calaresu F R
Department of Physiology, University of Western Ontario, London, Canada.
Am J Physiol. 1990 May;258(5 Pt 2):R1271-8. doi: 10.1152/ajpregu.1990.258.5.R1271.
Experiments were done to test the hypothesis that inhibition of neurons in the rostral ventrolateral medulla (RVLM) elicited by stimulation of the nucleus tractus solitarii (NTS) is relayed through the caudal ventrolateral medulla (CVLM). We recorded activity from 56 spontaneously firing units in the right RVLM of urethan-anesthetized and artificially ventilated rats. Eleven of these units were classified as cardiovascular neurons, because they were silenced by baroreceptor activation (1-3 micrograms phenylephrine iv) and showed rhythmicity of their spontaneous activity in synchrony with the cardiac cycle. Single pulses (0.1 ms, 30-75 microA) delivered 1/s to depressor sites in the ipsilateral NTS inhibited the activity of all these cardiovascular neurons. Microinjection of the glutamate antagonist kynurenic acid (0.15 M, 50 nl) into the ipsilateral CVLM blocked the inhibitory response of RVLM units to the administration of phenylephrine and increased the firing frequency of cardiovascular neurons in the RVLM by 43%. Moreover, kynurenic acid administration attenuated the inhibitory response of cardiovascular neurons in the RVLM to NTS stimulation. Finally, stimulation of the NTS that elicited depressor responses under control conditions produced a pressor response after kynurenic acid administration. The remaining 45 RVLM neurons were barosensitive but lacked cardiac cycle-related rhythmicity. These results provide direct evidence for the existence of a tonic inhibitory pathway from NTS to RVLM that is relayed through the CVLM probably by a glutamatergic projection from NTS to CVLM.
由孤束核(NTS)刺激引发的延髓头端腹外侧区(RVLM)神经元抑制是通过延髓尾端腹外侧区(CVLM)中继的。我们记录了经乌拉坦麻醉并人工通气的大鼠右侧RVLM中56个自发放电单位的活动。其中11个单位被归类为心血管神经元,因为它们在压力感受器激活(静脉注射1 - 3微克去氧肾上腺素)时沉默,并且其自发放电活动与心动周期同步呈现节律性。以1次/秒的频率向同侧NTS的降压位点施加单个脉冲(0.1毫秒,30 - 75微安)可抑制所有这些心血管神经元的活动。向同侧CVLM微量注射谷氨酸拮抗剂犬尿烯酸(0.15 M,50纳升)可阻断RVLM单位对去氧肾上腺素给药的抑制反应,并使RVLM中心血管神经元的放电频率增加43%。此外,给予犬尿烯酸可减弱RVLM中心血管神经元对NTS刺激的抑制反应。最后,在对照条件下引发降压反应的NTS刺激在给予犬尿烯酸后产生升压反应。其余45个RVLM神经元对压力敏感,但缺乏与心动周期相关的节律性。这些结果为存在从NTS到RVLM的紧张性抑制通路提供了直接证据,该通路可能通过从NTS到CVLM的谷氨酸能投射经CVLM中继。