1. 1.

    In the honey-bee drone retina (Apis mellifera) oxidative metabolism iscarried out largely by the photoreceptors. We have studied the effects of atransient inhibition of this metabolism, by recording receptor potentialsimultaneously with measurements of local Poo2 and extracellular [K+]([K+]o), using O2- and K+-sensitive microelectrodes.

  2. 2.

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

  3. 3.

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

  4. 4.

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

  5. 5.

    When O2 was reintroduced, or amytal washed out, oxidative metabolismrapidly resumed. [K+]o quickly decreased and, after a large undershoot, returned to the baseline in less than 5 min. There was in parallel arepolarization of the photoreceptors, followed by recovery of the receptorpotential.

  6. 6.

    About 5 min after reintroduction of O2, when the [K+]o, the membranepotential and the amplitude and kinetics of the receptor potential had completelyrecovered, exposure of the retina to a second anoxia suppressed thereceptor potential faster than had the first anoxia.

  7. 7.

    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 oflight recovered in parallel with the resistance to anoxia.

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