Abstract
Various Drosophila mutants were used to dissect the electroretinogram (ERG) frequency response into components of different origins. The ommochrome granules in the receptor cell body migrate in response to light, limiting the amount of light entering the rhabdomere. Comparison between the ERG frequency responses of the wild type and the mutant lacking the ommochrome granules indicates that the pigment migration reduces the amplitude gain at frequencies below 0.5 Hz. The ERG of Drosophila compound eyes consists of contributions from receptor cells and the 2nd-order cells in the lamina. Mutants with defective laminae showed a high-frequency cutoff with a corner frequency of about 20 Hz, while in wild type the response peaked in that frequency region. The lamina may contribute mainly to the high-frequency components of the ERG transfer function. The shot noise model was tested in Drosophila by comparing the frequency response of the genetically isolated receptor component and the power spectrum of the noise superimposed on the intracellular receptor potential. The receptor potential may consist of a summation of small discrete potentials (bumps). In a mutant in which the bumps exhibit latency dispersion in response to a dim flash, the receptor showed a poor high-frequency response, the corner frequency being lowered to about 1-2 Hz. The slope of the cutoff was approximately 20 dB/dec indicating that the latency dispersion in this mutant is the major limiting factor in temporal resolution. Light-evoked high frequency oscillations were observed in the ERG of another mutant. The oscillation was found sharply turned to light flickering at about 55 Hz.