Sakakibara M, Alkon D L, Kouchi T, Inoue H, Yoshioka T
Department of Biological Science and Technology, School of High Technology for Human Welfare, Tokai University, Numazu, Japan.
Biochem Biophys Res Commun. 1994 Jul 15;202(1):299-306. doi: 10.1006/bbrc.1994.1927.
Direct evidence that the photoresponse of the Hermissenda type B photoreceptor cell is triggered directly by the hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) was obtained. Neomycin and spermine, which inhibit PIP2 breakdown, suppressed light response, while injection of inositol 1,4,5-trisphosphate (IP3), guanosine 5'-(3-O-thio)triphosphate (GTP gamma S), guanosine 5'-(2-O-thio)diphosphate (GDP beta S), cAMP, cGMP did not alter the light-induced Na+ influx underlying the photoresponse. Suppression of the photoresponse was also observed with decrease of total amount of membraneous PIP2 induced by injection of the phosphoinositides (PI) turnover inhibitors, isobutylmethylxanthine (IBMX), LiCl and R 59022.
已获得直接证据表明，海兔B型光感受器细胞的光反应是由磷脂酰肌醇4,5-二磷酸（PIP2）水解直接触发的。抑制PIP2分解的新霉素和精胺可抑制光反应，而注射肌醇1,4,5-三磷酸（IP3）、鸟苷5'-(3-O-硫代)三磷酸（GTPγS）、鸟苷5'-(2-O-硫代)二磷酸（GDPβS）、环磷酸腺苷（cAMP）、环磷酸鸟苷（cGMP）并不会改变光反应所依赖的光诱导Na+内流。注射磷酸肌醇（PI）周转抑制剂异丁基甲基黄嘌呤（IBMX）、氯化锂和R 59022导致膜PIP2总量减少，也观察到了光反应的抑制。
