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.

A large cell to cell variability of the prolonged depolarizing afterpotential (PDA) decay time constant (tau) has been measured in Balanus eberneus lateral ocelli. While 25% of the cells had PDA's of long duration, tau greater than 10 min. 45% of the cells tested showed either weak (tau less than 60 s) PDA or none at all. The variability was not reflected in the late receptor potential. All the cells showed normal light-coincident responses. The variability was not due to some alteration of the thermal stability of the pigment states, since after monochromatic adaptation the amplitude of the early receptor potential remained unchanged for at least 30 min. In addition, in some cells that initially showed PDAs of long duration, the decay time was either shortened or abolished after exposure to anoxia. Again, the late receptor potential and the stability of the pigments remained unaffected. These results indicate that the mechanisms which give rise to the PDA are not always tightly coupled to the direct chain of events that lead to the light-coincident response.