The effects of anoxia, 2,4-dinitrophenol (DNP), and carbon dioxide (CO2) on the late receptor potential of Balanus lateral ocelli, Limulus ventral eyes, and the retinular cells of Linulus lateral eyes have been studied. Either anoxia, DNP, or exposure to 100% CO2 causes a depolarization of 5-30 mV and a gradual reduction and eventually abolition of the late receptor potential and an increase in the latency and time to peak of the response. This lengthening of the time scale is in contrast to the response obtained in photoreceptors that have been light-adapted or injected with calcium. In that case a loss in sensitivity is associated with a decrease in latency and time to peak. Because of these observed differences, the effects of metabolic inhibition cannot be attributed merely to a loss in regulation of intracellular free calcium. Rather, because alteration of intracellular pH (pHi) by using either (NH4)2SO4 or CO2 produced changes in the photoresponse similar to those caused by metabolic inhibition, it is suggested that changes in pHi during metabolic inhibition can account in part for the lengthening of the time scale. In addition to the changes in pHi and internal Ca++ concentration due to metabolic inhibition, the possible role of other consequences of metabolism in the transduction mechanism is also discussed.

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