Coleman M J, Dampney R A
Department of Biomedical Sciences, University of Sydney, New South Wales, Australia.
Am J Physiol. 1998 Feb;274(2):R318-23. doi: 10.1152/ajpregu.1998.274.2.R318.
The present study was performed to determine whether the powerful depressor and sympathoinhibitory response that can be evoked from neurons in the caudal midline medulla is mediated by gamma-aminobutyric acidergic (GABAergic) inhibition of sympathoexcitatory neurons in the rostral part of the ventrolateral medulla (VLM). In anesthetized barointact and barodenervated rabbits, bilateral micro-injections of bicuculline into sympathoexcitatory sites in the rostral VLM resulted in a sustained increase in renal sympathetic nerve activity and abolished or reversed the depressor and sympathoinhibitory response evoked by glutamate micro-injection into the caudal midline medulla. By contrast, the sympathoinhibitory response evoked from the caudal midline medulla persisted when the background level of renal sympathetic nerve activity was reflexly raised by baroreceptor unloading. The results indicate that 1) the depressor and sympathoinhibitory response evoked by stimulation of neurons in the caudal midline medulla is mediated by a GABAergic synapse in the rostral VLM and 2) there are also sympathoexcitatory neurons in the caudal midline medulla whose presence is revealed by blockade of the more powerful sympathoinhibitory response.
本研究旨在确定从延髓尾侧中线神经元诱发的强大降压和交感抑制反应是否由γ-氨基丁酸能(GABA能)对延髓腹外侧部(VLM)头端交感兴奋神经元的抑制介导。在麻醉的压力感受性反射完整和压力感受性反射神经切除的家兔中,向VLM头端的交感兴奋部位双侧微量注射荷包牡丹碱导致肾交感神经活动持续增加,并消除或逆转了向延髓尾侧中线微量注射谷氨酸所诱发的降压和交感抑制反应。相比之下,如果通过压力感受器卸载反射性提高肾交感神经活动的背景水平,从延髓尾侧中线诱发的交感抑制反应则持续存在。结果表明:1)刺激延髓尾侧中线神经元所诱发的降压和交感抑制反应是由VLM头端的GABA能突触介导的;2)延髓尾侧中线也存在交感兴奋神经元,其存在通过阻断更强的交感抑制反应得以揭示。