Ikeuchi Y, Nishizaki T
Department of Physiology, Kobe University School of Medicine, Japan.
Biochem Biophys Res Commun. 1995 Sep 14;214(2):589-96. doi: 10.1006/bbrc.1995.2326.
In whole-cell patches of inferior colliculus neurons, ADP evoked outwardly rectifying potassium currents with a latency of < 1 sec via P2Y purinoceptor. These currents were blocked by GDP beta S, while not by pertussis toxin (PTX). Additionally, a selective protein kinase C inhibitor, GF109203X, or a selective phospholipase A2 inhibitor, BPB, had no effect on the currents. In outside-out patches, ADP elicited single channel currents with same slope conductances as those obtained in cell-attached patches and the currents were again blocked by GDP beta S. The results presented here indicate that the P2Y purinoceptor-operated potassium channel in inferior colliculus neurons is activated only by a plasma membrane component, most likely by a direct coupling to the beta gamma subunits of a PTX-insensitive G-protein.
在下丘神经元的全细胞膜片中,ADP通过P2Y嘌呤受体诱发外向整流钾电流,潜伏期<1秒。这些电流被GDPβS阻断,但不被百日咳毒素(PTX)阻断。此外,选择性蛋白激酶C抑制剂GF109203X或选择性磷脂酶A2抑制剂BPB对电流无影响。在外面向外的膜片中,ADP诱发的单通道电流与在细胞贴附膜片中获得的电流具有相同的斜率电导,并且电流再次被GDPβS阻断。此处给出的结果表明,下丘神经元中P2Y嘌呤受体激活的钾通道仅由质膜成分激活,很可能是通过与PTX不敏感G蛋白的βγ亚基直接偶联激活的。