Roles of cyclic GMP and inositol triphosphate in phototransduction of the molluscan extraocular photoreceptor

Abstract

The internal messengers mediating the photocurrent of the molluscan extraocular photoreceptor, A-P-1, were examined. In the dark, pressure-injection of cGMP into the A-P-1, voltage-clamped at resting levels, produced a rapid outward current, associated with an increase in conductance. However, the cGMP-induced current and increase in conductance were suppressed by subsequent photostimulation, suggesting hydrolysis of cGMP by light. The steady-state I/V relation for the cGMP-induced current was non-linear. The I/V relation for the instantaneous cGMP-induced current, measured 50 ms after the beginning of a voltage step, was linear, and reversed at the menbrane potential, −67 mV, which corresponded to the K + equilibrium potential of A-P-1 in 10 mM K + normal saline. These findings indicate that the internal cGMP induces a voltage- and time-dependent K + current. Since the photocurrent results from the suppression of a voltage- and time-dependent K + current similar to above, the photocurrent is considered to be equivalent to the supression of the cGMP-induced current. Short pressure-injection of GDP-β-S into A-P-1 reduced the subsequent photocurrent. The photocurrent was also suppressed after an external application of Pertussis toxin. On the other hand, the photocurrent was amplified by prior pressure-injection of inositol 1,4,5-traiphosphate (IP 3). However, a short pressure-injection of neomycin into A-P-1 depressed the subsequent photocurrent. These results suggested that the cGMP-induced (dark) current is mediated by cGMP, and that hydrolysis of cGMP by light leads to the photocurrent, then being modified by another messenger, IP 3 to be amplified. In addition, the photocurrent seems to originate in an early enzymatic step, T-GTP in the phototransduction.