Light-increased cGMP and K+ conductance in the hyperpolarizing receptor potential of Onchidium extra-ocular photoreceptors.
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.
Nishi
T
T
Laboratory of Physiology, Senshu University, Kawasaki, Japan.
Gotow
T
T
D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D015761:4-Aminopyridine / Q000494:pharmacology; D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000005:Abdomen / Q000294:innervation; D000634:Aminoquinolines / Q000494:pharmacology; D000818:Animals; D006152:Cyclic GMP / Q000037:antagonists & inhibitors / Q000378:metabolism*; D004553:Electric Conductivity; D004594:Electrophysiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D008974:Mollusca; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D010775:Photic Stimulation; D017956:Photoreceptor Cells, Invertebrate / Q000737:chemistry* / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D011688:Purinones / Q000494:pharmacology; D015290:Second Messenger Systems / Q000502:physiology; D019789:Tetraethylammonium / Q000494:pharmacology; D014785:Vision, Ocular / Q000502:physiology*
D000634:Aminoquinolines; D004791:Enzyme Inhibitors; D010726:Phosphodiesterase Inhibitors; D011688:Purinones; D015124:8-Bromo Cyclic Adenosine Monophosphate; D019789:Tetraethylammonium; C041715:6-anilino-5,8-quinolinedione; D015761:4-Aminopyridine; C011145:zaprinast; D006152:Cyclic GMP; D011188:Potassium; D015056:1-Methyl-3-isobutylxanthine