The Recovery From a Transient Inhibition of the Oxidative Metabolism of the Photoreceptors of the Drone (Apis Mellifera ♂) Available to Purchase

In the honey-bee drone retina (Apis mellifera) oxidative metabolism is carried out largely by the photoreceptors. We have studied the effects of a transient inhibition of this metabolism, by recording receptor potential simultaneously with measurements of local and extracellular [K⁺] ([K⁺]_o), using O₂-and K⁺-sensitive microelectrodes.

When the retina was subjected to anoxia or exposed to Na-amobarbital (amytal), the photoreceptors depolarized by about 30 my, in parallel with an increase of [K⁺]_o of up to 30 mmol 1⁻¹, and the receptor potential was abolished in 2–3 min.

The reduction of the receptor potential followed the beginning of anoxia with a delay, which we define as a ‘resistance’ of the photoreceptors to anoxia.

The resistance to anoxia was greater if the photoreceptors were stimulated with only low intensity light flashes, suggesting that the effects of anoxia are due to the progressive consumption of a substance stored in the photoreceptors. This substance is probably ATP.

When O₂ was reintroduced, or amytal washed out, oxidative metabolism rapidly resumed. [K⁺]_o quickly decreased and, after a large undershoot, returned to the baseline in less than 5 min. There was in parallel a repolarization of the photoreceptors, followed by recovery of the receptor potential.

About 5 min after réintroduction of O2, when the [K⁺]_o, the membrane potential and the amplitude and kinetics of the receptor potential had completely recovered, exposure of the retina to a second anoxia suppressed the receptor potential faster than had the first anoxia.

Full recovery of the resistance to anoxia thus takes longer (by about 10 min) than recovery of the electrical properties of the photoreceptor cells. The amplitude of the extra oxygen consumption measured after a flash of light recovered in parallel with the resistance to anoxia.