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 Ca 2+ 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.