RESCUE OF EXCITATION BY INOSITOL FOLLOWING LI-INDUCED BLOCK IN LIMULUS VENTRAL PHOTORECEPTORS()

The phosphoinositide (PI) intracellular signaling pathway, which trigg ers Ca2+ release from intracellular stores, appears to be a central fe ature of phototransduction in most invertebrate species studied. Proce dures designed to inhibit PI-pathway reactions cause suppression of ex citation to dim lights. However, in Limulus photoreceptors, responses to bright stimuli are in fact enhanced by some of these procedures, su ggesting that PI metabolism is not obligatory for Light-induced excita tion. Other studies, however, suggest that Ca2+ release is obligatory for excitation. We studied this issue by examining the effects of PI-p athway inhibitor, Li+, on electrophysiological responses to light in L imulus photoreceptors. Li+ is reported to cause depletion of intracell ular PI-pathway intermediate, inositol; and it offers the pharmacologi cal advantage that its block can be bypassed by introducing exogenous inositol. Introduction of Li+ caused a very slowly developing but comp lete suppression of responses to dim stimuli. In contrast, Li+ caused a rapidly developing but partial suppression of responses to bright st imuli. Li+-induced suppression was reversed by exogenous introduction of inositol. In addition, inositol prevented Li+-induced suppression o f excitation. Li+ enhanced light adaptation (light-induced desensitiza tion) but slowed response deactivation, indicating a difference in the processes underlying these phenomena. Li+ slowed dark adaptation, the recovery of sensitivity following Light adaptation. All of these effe cts were prevented or rescued by extracellularly applied inositol, sug gesting the presence of a transmembrane inositol transport system. The overall results suggest that PI-dependent signaling is central and ob ligatory for excitation in Limulus, at least for responses to dim to m oderate illumination. The failure of Li+ to suppress bright light-indu ced excitation completely may be due to a failure of Li+ to block PI m etabolism completely, as in other systems; however, it may point to a parallel, PI-independent excitation pathway possessing very low light sensitivity when PI metabolism is inhibited.