Fluoride blocks an inactivation step of transduction in a locust photoreceptor.

1. Photoreceptors in a superfused retina of a locust compound eye are treated with saline containing 10 mM-NaF, while their intracellular resting potential and responses are recorded using glass micropipettes.2. Treatment for two minutes with 10 mM-NaF, followed by a series of brief, bright flashes of light, results in an irreversible, noisy depolarization of approximately 10 mV. The final, stable level of depolarization is reached through the summed effect of each of the noisy, depolarizing afterpotentials that follow every response of the cell to a light flash. If kept in darkness after treatment with NaF, the noisy depolarization still develops, but more gradually, over a period of 5 min.3. The voltage noise induced by NaF mimics light-induced voltage noise when the two are compared at mean depolarizations of more than 15 mV. At very small depolarizations, however, fluoride-induced noise cannot be resolved into the large discrete events (bumps) that are typical of the response of a dark-adapted photoreceptor to a single photon.4. The complete replacement of the superfusate sodium by choline reversibly reduces the fluoride-induced noise and depolarization to the same extent as it does the light-induced noise and depolarization of an illuminated cell.5. Increasing the superfusate calcium concentration from 0.5 to 10 mM also reversibly reduces fluoride-induced noise and depolarization to the same extent as it does light-induced noise and depolarization. This action of calcium is accompanied by an increase in a cell's input resistance which opposes the reduction caused by light or fluoride treatment.6. The results confirm the proposal (Payne, 1981) that anionic metabolic inhibitors cause spontaneous activity in sodium channels that are normally opened by light. A model is proposed in which fluoride acts by blocking the inactivation of a late stage in the transduction mechanism.