Guan B C, Li Z W, Zhou X P
Research Centre of Experimental Medicine, Tongji Medical University, Wuhan.
Sheng Li Xue Bao. 1994 Oct;46(5):441-50.
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 x 10(-6)-4 x 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.
对幼鼠背根神经节(DRG)神经元进行细胞内记录,以研究P物质(SP)对由γ-氨基丁酸A(GABAA)受体和γ-氨基丁酸B(GABAB)受体介导的反应的调节作用。在大多数神经元(20/30)中,预先应用SP(5×10⁻⁶ - 4×10⁻⁵mol/L)可使GABA诱导的去极化抑制至50.8±20.2%,单独应用SP则无作用或仅引起轻微去极化。此外,在许多神经元(10/18)中,SP可使动作电位时程50%(APD50)增加28.7±9.1%,预先应用SP可消除(4/12)或甚至使巴氯芬诱导的APD50缩短20.6±2.9%逆转至APD50延长19.3±8.9%(8/12)。此外,还发现GABAB受体的激活可抑制随后由GABAA受体介导的反应。由于DRG神经元的胞体通常被认为是初级传入终末的一个可接近模型,这些结果表明,在伤害性刺激期间于背角释放的SP可拮抗由GABAA受体和GABAB受体介导的反应。