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在急性分离的大鼠背根神经节 (dorsalrootganglion ,DRG)细胞上 ,应用全细胞膜片箝技术观察了预加催产素 (oxytocin ,OT)对GABA激活电流的调制作用。结果如下 :(1)大多数细胞 (4 8/ 5 2 ,90 5 % )对GABA敏感。(2 )OT可引起 5 1 3% (2 0 / 39)的受检细胞出现外向膜电流 ;43 6 % (17/ 39)无明显膜反应 ;5 1% (2 / 39)出现内向膜电流。 (3)预加OT (10 -12 ～ 10 -9mol/L) 30～ 90s后 ,大部分GABA激活电流增加 (33/ 39,84 6 % ) ;少数无明显反应(4 / 39,10 3% )或略有抑制 (2 / 39,5 1% )。GABA (10 -4 mol/L)增强作用为浓度依赖性的 ,在OT浓度为 10 -12 、10 -11、10 -10 、10 -9mol/L时 ,GABA激活电流的增强分别为 :2 4 1± 7 6 % (n =6 ) ,33 4± 6 9% (n =9) ,40 2±6 5 % (n =13) ,6 7 2± 14 8% (n =5 )。当OT浓度升高 (10 -8及 10 -7mol/L)时 ,GABA激活电流不但不增高 ,反而被抑制。 (4 )预加OT后 ,GABA激活电流量 效曲线的Kd值降低 ,最大反应浓度增加。(5 )预加OT和未预加OT的电流 电压曲线显示 ,其翻转电位均在 0mV左右。以上结果提示 :OT受体激活后可能通过相应的胞内转导机制增强GABA激活电流 ,从而在初级感觉神经元水平加强GABA的突触前抑制作用而减弱感觉信息的传递
Whole cell patch clamp technique was used to observe the modulating effect of oxytocin (OT) on GABA-activated current in acutely isolated rat dorsal root ganglion (DRG) cells. The results were as follows: (1) Most cells (48/52, 905%) were sensitive to GABA. (2) OT could cause outward membrane current in 51.3% (20/39) of the tested cells; 43.6% (17/39) had no obvious membrane reaction; 5 1% (2/39) appeared inward membrane current . (3) Pretreatment with OT increased the activation current of GABA (33/39, 84 6%) after 30-90 s; few had no obvious response (4/39, 10 3% ) Or slightly inhibited (2/39, 51%). The enhancement of GABA (10 -4 mol / L) concentration was concentration-dependent. The enhancement of GABA activation current at OT concentrations of 10 -12, 10 -11, 10 -10, 10 -9 mol / 1 ± 7 6% (n = 6), 33 4 ± 6 9% (n = 9), 40 2 ± 65% (n = 13) and 6 7 2 ± 14 8% (n = 5). When OT concentration increased (10 -8 and 10 -7 mol / L), GABA activation current not only increased, but was inhibited. (4) After pretreatment with OT, the Kd value of GABA-activated current dose-response curve decreased and the maximum response concentration increased. (5) The curves of current and voltage of pre-OT and non-pre-OT show that the reversal potentials are about 0mV. The above results suggest that the activation of OT receptor may enhance the GABA activation current through the corresponding intracellular transduction mechanism and thus reduce the presynaptic inhibition of GABA at the level of primary sensory neurons and reduce the transmission of sensory information