RUTHENIUM RED BLOCKS THE CAPSAICIN-INDUCED INCREASE IN INTRACELLULAR CALCIUM AND ACTIVATION OF MEMBRANE CURRENTS IN SENSORY NEURONS AS WELL AS THE ACTIVATION OF PERIPHERAL NOCICEPTORS INVITRO
RUTHENIUM RED BLOCKS THE CAPSAICIN-INDUCED INCREASE IN INTRACELLULAR CALCIUM AND ACTIVATION OF MEMBRANE CURRENTS IN SENSORY NEURONS AS WELL AS THE ACTIVATION OF PERIPHERAL NOCICEPTORS INVITRO
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DOI：
10.1016/0304-3940(90)90786-9
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发表时间：
1990-03-02
影响因子：
2.5
通讯作者：
BURGESS, GM
中科院分区：
文献类型：
--
作者：
DRAY, A;FORBES, CA;BURGESS, GM
在一些感觉神经元制剂中，钌红(RR)选择性地减弱了对辣椒素的反应。首先，RR(100 NM)可逆地阻断辣椒素而不是缓激肽引起的[Ca~(2+)]i升高，但可逆地阻断辣椒素激活的单离子通道电流。RR的这种效应不同于La所产生的效应。最后，在体外维持的新生大鼠脊髓尾部标本中，RR选择性地减弱辣椒素产生的外周伤害性感受器的激活，而不是由缓激肽或伤害性高温产生的。这些数据表明，RR通过在质膜上阻止辣椒素激活的离子通道开放来抑制辣椒素对感觉神经元的影响。
In a number of sensory neurons preparations, Ruthenium red (RR) selectively attenuated the response to capsaicin. First, RR (100 nM) reversibly abolished capsaicin but not bradykinin induced increases in [Ca2+]i measured but reversibly abolished capsaicin-activated single ion channel currents measured in membrane patches from rat DRG neurons. This effect of RR differed from that produced by lanthanum. Finally, in a neonatal rat spinal cord-tail preparation maintained in vitro, RR selectively attenuated the activation of peripheral nociceptors produced by capsaicin but not by bradykinin or noxious heat. These data indicate that RR inhibits capsaicin mediated effects on sensory neurons by an action on the plasma membrane to prevent opening of capsaicin activated ion channels.