17β-雌二醇对大鼠海马神经元延迟整流型钾离子通道活动的影响

EFFECTS OF 17β-ESTRADIOL ON DELAYED RECTIFIER POTASSIUM CHANNELS IN HIPPOCAMPAL PYRAMIDAL NEURONS OF THE RAT

用膜片箝技术的细胞贴附式和内面向外式，研究17β-雌二醇（E2）对大鼠海马神经元延迟整流型K+通道的影响。结果表明，1．0和10．0nmol／LE2可分别使42pSK+通道开放概率由（67．4t18．2）％下降到（41．22±12．5）％和由（56．3±15．8）％下降到（13，2±12．6）％，通道开放频率由（43．40±6．7）Hz下降到（27．68±9．1）Hz和由（38．19±10．1）Hz下降到（15．79±3．5）Hz，通道平均开放时间缩短，平均关闭时间延长，但通道电流幅度无显著改变，提示E2对海马神经元42pSK+通道的活动具有抑制作用，这种作用可能是激素直接作用于细胞膜的结果。

In the present study, both cell-attached and inside-out patch-clamp techniques wereused to detect the effects of 17β-estradiol (E2) on 42 pS delayed rectifier potassiumchannels in acutely dissociated hippocampal neurons of new-born SD rats. The resultsindicated that after application of 1 .0 and 10.0 nmol/L E2, the open probabilities of K+channels were decreased from (67.4 ± 18.2) % to (41 .2 ± 12.5) % and from (56.3 ±15.8) % to (13.2 ± 12.6) % respectively, the open frequencies were reduced from(43.40 ± 6.7) Hz to (27.68 ± 9. 1) Hz and from (38. 19 ± 10. 1) Hz to (15.79 ± 3.5)Hi respectively. Meanwhile, there was a shortening of the mean open time and alenghtening of the mean close time of the channels. The above results suggest that E2 hassuppressive effects on the activities of the channels, which might be exerted through adirect action on the cellular membrane.