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DOI:
https://doi.org/10.5007/%25xAbstract
A revision of electroretinogram studies conducted in the eye of insects (Hypmenoptera: Formicoidea) is presented showing that the response to light should be understood as a result of the action of two opposinf processes: Facilitation and adaptation. These studies raised the questions examined in the present work: 1) If facilitation occurs in insect photoreceptor cells and 2) What are the mechanisms that explain this phenomenon. Intracellular responses of photoreceptors of the compound eyes of the stingless bee Melipona quadrifsciata and of the locust Schistocerca sp. were studied in order to determine: a) The time course of facilitation, with trains of light pulses presented at different interflash intervals, or varying the duration of a light stimulus, b) The effect of light intersity, c) The relationship between latency of the receptor potential and facilitation, and d) Possible mechanisms: synaptic influences, metarhodopsin, physiological condition of the preparation, the second messenger InsP3. The results showed that 1) Facilitation occurs in insect photoreceptors for light stimuli of high intensity and short duration, and it is greater in the photoreceptor of locusts than in the bee, b) Its temporal course is similar to that found with the ERG, 3) There is no relationship between the amplitude and the latency of facilitated receptor potentials, 4) Facilitation is directly proportional to the hyperpolatizing after potential found with high intensity illumination, 5) Recordings in the eye of the bee Melipona quadrifasciata showed that synaptic and metarhodopsin influences can be excluded, and that facilitation is not due to impairment of the physiological conditions of the preparation, on the contrary, it disappears in those conditions. Experiments with InsP3 and DPG yielded inconclusive results due to technical difficulties. The results were discussed in the light of the present knowledge about transduction in photoreceptors, which suggest that facilitation could be due to an accumulation of the second transmitter in the cell.Downloads
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1992-01-01
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