Heesch Cheryl M, Laiprasert Jennifer D, Kvochina Lyudmyla
Dept. Biomed. Sci. and Dalton Cardiovascular Res. Ctr., University of Missouri, Dalton Cardiovascular Research Center, 134 Research Park Dr., Columbia, MO 65211, USA.
Brain Res. 2006 Dec 13;1125(1):46-59. doi: 10.1016/j.brainres.2006.09.090. Epub 2006 Nov 16.
The caudal ventrolateral medulla (CVLM) provides tonic inhibitory and also excitatory inputs to the rostral ventrolateral medulla (RVLM). These experiments evaluated the role of RVLM gamma-amino butyric acid (GABA) receptor subtypes and glycine receptors in mediating CVLM sympathoinhibition. In Inactin anesthetized female rats, the CVLM and RVLM were functionally defined by pressor and depressor responses to microinjected GABA (500 pmol, 50 nl). Although reduced, pressor and sympathoexcitatory responses due to inhibition of the CVLM with GABA persisted following ipsilateral RVLM GABA(A) receptor blockade (bicuculline, BIC, 400 pmol, 100 nl; n=12) in rats with contralateral nucleus tractus solitarius (NTS) lesion. In the presence of either ipsilateral (+contralateral NTS lesion; n=8) or bilateral (n=6) GABA(A) and GABA(B) receptor blockade of the RVLM (400 pmol BIC+400 pmol CGP35348, 100 nl), inhibition of the CVLM still increased MAP and renal sympathetic nerve activity (RSNA). Thus neither GABA(B) receptors nor a contralateral CVLM to RVLM GABAergic pathway explains residual responses to CVLM blockade. The addition of strychnine (300 pmol, 100 nl) to the RVLM eliminated responses to CVLM inhibition, suggesting that a GABA(A) and GABA(B) independent sympathoinhibitory influence from CVLM to RVLM is mediated by glycine receptors. Decreases in MAP and RSNA due to activation of the CVLM with glutamate (500 pmol, 50 nl) were reversed to increases in the presence of RVLM GABA(A) receptor blockade (n=7). Thus, a sympathoexcitatory pathway from the CVLM can be activated in the presence of RVLM GABA receptor blockade, but sympathoinhibitory influences from the CVLM predominate.
尾侧腹外侧延髓（CVLM）向头侧腹外侧延髓（RVLM）提供持续性抑制性输入以及兴奋性输入。这些实验评估了RVLMγ-氨基丁酸（GABA）受体亚型和甘氨酸受体在介导CVLM交感神经抑制中的作用。在使用氯醛糖麻醉的雌性大鼠中，通过对微量注射GABA（500皮摩尔，50纳升）的升压和降压反应来功能性地定义CVLM和RVLM。在对侧孤束核（NTS）损伤的大鼠中，尽管由于用GABA抑制CVLM导致的升压和交感神经兴奋反应有所减弱，但在同侧RVLM GABA(A)受体阻断（荷包牡丹碱，BIC，400皮摩尔，100纳升；n = 12）后仍持续存在。在同侧（+对侧NTS损伤；n = 8）或双侧（n = 6）RVLM的GABA(A)和GABA(B)受体阻断（400皮摩尔BIC + 400皮摩尔CGP35348，100纳升）的情况下，抑制CVLM仍会增加平均动脉压（MAP）和肾交感神经活动（RSNA）。因此，GABA(B)受体和从对侧CVLM到RVLM的GABA能通路都不能解释对CVLM阻断的残余反应。向RVLM添加士的宁（300皮摩尔，100纳升）消除了对CVLM抑制的反应，表明从CVLM到RVLM的一种独立于GABA(A)和GABA(B)的交感神经抑制作用是由甘氨酸受体介导的。由于用谷氨酸（500皮摩尔，50纳升）激活CVLM导致的MAP和RSNA降低，在RVLM GABA(A)受体阻断的情况下（n = 7）逆转增加。因此，在RVLM GABA受体阻断的情况下，可以激活从CVLM的交感神经兴奋通路，但来自CVLM的交感神经抑制作用占主导。
