MODULATION OF THE VOLTAGE-GATED SODIUM AND CALCIUM CHANNELS BY PERTUSSIS TOXIN SENSITIVE Gi PROTEIN IN NEURONS ISOLATED FROM COTTON BOLLWORM (Helicoverpa armigera)
百日咳毒素对棉铃虫神经细胞电压门控钠、钙通道的调节作用

The modulation of voltage-gated sodium and calcium channels by pertussis toxin (PTX) sensitive Gi protein in the central neurons isolated from three instar larve of the Helicoverpa armigera was studied using whole-cell patch clamp technique. Sodium channels were activated when the membrane potential was depolarized to -50~-40 mV and the current reached peak value at about -20 mV in control. During the 20 min of recording, little change was shown in I-V relationship curves and peak value as well. Pretreated with pertussis toxin, however, sodium channels were activated at about -40 mV and current reached peak value at about 0 mV. Moreover, the I-V curve was continually shifted in positive direction during the recording. In addition, the peak current decreased to (70.92±8.76)% of initial peak value by the end of 20 min recording. Calcium channels were activated when the membrane was depolarized to -40~-30 mV and the current was maximized at about 0 mV in control. After treatment with PTX, I-V curve was shifted approximately 10 mV in negative direction and the shift was continued during the period of recording. Rundown in current was more apparent than that in control. The time course to reach peak current for calcium channels was obviously prolonged by PTX treatment. Taken together, the results suggested that Gi protein modulates voltage sensitivity and open probability of sodium and calcium channels via direct or indirection pathways, and affects the rate of gating from closed state to the active in calcium channels. Furthermore, it was noticeable that the I-V shift of sodium channel in PTX-treated neurons was significantly similar to that of resistant cotton bollworm, which indicated that Gi protein might participate in the evolution of resistance to insecticide.