P物质对GABA_A和GABA_B受体介导的DRG神经元膜反应的调制作用

MODULATORY EFFECTS OF SUBSTANCE P ON THE MEMBRANE RESPONSES MEDIATED BY GABA_A AND GABA_B RECEPTORS IN DRG NEURONS

实验在幼年大鼠ＤＲＧ标本上进行。应用细胞内记录观察了ＳＰ对ＧＡＢＡ反应的调制作用。结果证明：（１）单独滴加ＳＰ（５×１０（－６）－４×１０（－５）ｍｏｌ／Ｌ）或浴槽灌流ＳＰ（１０（－６）－５×１０（－６）ｍｏｌ／Ｌ）不引起膜电位的改变或仅有轻微的去极化，但却能使ＧＡＢＡ引起的去极化反应减小５０．８±２０．２％（±ＳＤ）（２０／３０）；（２）单独滴加ＳＰ可使多数受检细胞ＡＰＤ５０延长２８．７±９．１％（±ＳＤ）（１０／１８）；（３）在预加ＳＰ后，能使ｂａｃｌｏｆｅｎ所引起的ＡＰＤ５０缩短效应（２０．６±２．９％，±ＳＤ）完全消除（４／１２）或翻转成ＡＰＤ（５０）延长１９．３±８．９％（±ＳＤ）（８／１２）；（４）预加ＧＡＢＡＢ受体激动剂ｂａｃｌｏｆｅｎ（１０（－４）－１０（－３）ｍｏｌ／Ｌ）３０—９０ｓ后明显地抑制ｍｕｓｃｉｍｏｌ（１０－４－１０－３ｍｏｌ／Ｌ）引起的去极化反应，其抑制效应达５４．４±１８．８％（±ＳＤ）（１７／２０）。由于ＤＲＧ神经元的胞体通常可用来作为研究初级传入终末的模型，因而本文实验结果提示：介导伤害性刺激信息的Ｐ物质在背角的释放，可能作用于初级传入终末，从而产生对抗ＧＡＢＡ介导的突触?

Intracellular recordings were performed on the neurons of young rat DRG to study the modulatory effects of SP on the responses mediated by GABAA and GABAB receptors. In the majority of the neurons (20/30) the GABA induced depolarization was suppressed to 50. 8 ± 20. 2% by preapplication of SP (5×10-6-4×10-5 mol/L),which applied alone had no effect or only caused a slight depolarization.In addition,SP could increase APD50 by 28. 7 ± 9. 1 % in many neurons (10/18), and the baclofen-induced shortening of 20. 6 ± 2. 9 % in APD50 could abolished (4/12) or even reverse to a lengthening of 19. 3 ±8. 9 % in APD50 (8/12) by the preapplication of SP. Moreover, it was found that the activation of GABAB receptors could inhibit the succeeding response mediated by GABAA receptors. Since the soma of . the DRG neuron is generally considered as an accessible model for the primary afferent terminals, the results suggest that SP which is released in the dorsal horn during nociceptive stimulation can antagonize the responses mediated by GABAA and GABAB receptors.