Nishi T, Gotow T
Laboratory of Physiology, Senshu University, Kawasaki, Japan.
Brain Res. 1998 Nov 2;809(2):325-36. doi: 10.1016/s0006-8993(98)00913-5.
The phototransduction mechanism of the extra-ocular photoreceptor cells Ip-2 and Ip-1 in the mollusc Onchidium ganglion was examined. Previous work showed that the depolarizing receptor potential of another extra-ocular photoreceptor cell, A-P-1 is produced by a decrease of the light-sensitive K+ conductance activated by a second messenger, cGMP and is inactivated by the hydrolysis of cGMP. Here, a hyperpolarizing receptor potential of Ip-2 or Ip-1 was associated with an increase in membrane conductance. When Ip-2 or Ip-1 was voltage-clamped near the resting membrane potential, light induced an outward photocurrent corresponding to the above hyperpolarization. The spectral sensitivity had a peak at 510 nm. The shift of reversal potentials of the photocurrent depended on the Nernst equation of K(+)-selective conductance. The photocurrent was blocked by 4-AP and L-DIL, which are effective blockers of the A-P-1 light-sensitive K+ conductance. These results suggested that the hyperpolarization is mediated by increasing a similar light-sensitive K+ conductance to that of A-P-1. The injection of cGMP or Ca2+ into a cell produced a K+ current that mimicked the photocurrent. 4-AP and L-DIL both abolished the cGMP-activated K+ current, while TEA suppressed only the Ca(2+)-activated K+ current. These results indicated that cGMP is also a second messenger that regulates the light-sensitive K+ conductance. The photocurrent was blocked by LY-83583, a guanylate cyclase (GC) inhibitor, but was unaltered by zaprinast, a phosphodiesterase (PDE) inhibitor. Together, the present results suggest that increasing the internal cGMP in Ip-2 or Ip-1 cells light-activates GC rather than inhibits PDE, thereby leading to an increase of the light-sensitive K+ conductance and the hyperpolarization.
对软体动物背角无齿蚌神经节中眼外光感受器细胞Ip - 2和Ip - 1的光转导机制进行了研究。先前的研究表明，另一种眼外光感受器细胞A - P - 1的去极化受体电位是由第二信使环鸟苷酸（cGMP）激活的光敏感钾离子电导降低产生的，并且通过cGMP的水解而失活。在这里，Ip - 2或Ip - 1的超极化受体电位与膜电导增加有关。当Ip - 2或Ip - 1在静息膜电位附近进行电压钳制时，光诱导出与上述超极化相对应的外向光电流。光谱敏感性在510nm处有一个峰值。光电流反转电位的变化取决于钾离子选择性电导的能斯特方程。光电流被4 - 氨基吡啶（4 - AP）和利多卡因（L - DIL）阻断，这两种物质是A - P - 1光敏感钾离子电导的有效阻断剂。这些结果表明，超极化是通过增加与A - P - 1类似的光敏感钾离子电导介导的。向细胞内注射cGMP或钙离子会产生一种模拟光电流的钾离子电流。4 - AP和L - DIL都消除了cGMP激活的钾离子电流，而四乙铵（TEA）仅抑制钙离子激活的钾离子电流。这些结果表明，cGMP也是调节光敏感钾离子电导的第二信使。光电流被鸟苷酸环化酶（GC）抑制剂LY - 83583阻断，但不受磷酸二酯酶（PDE）抑制剂扎普司特的影响。总之，目前的结果表明，增加Ip - 2或Ip - 1细胞内的cGMP会使GC光激活而非抑制PDE，从而导致光敏感钾离子电导增加和超极化。
