Electroretinography (ERG) of adult Adcy1(brl) mutant mice, which are deficient in adenylyl cyclase type 1 (AC1) activity, revealed decreased amplitude of the oscillatory potentials (OP) and of the primary rising phase of the b-wave intensity-response function in scotopic conditions. These abnormalities were less discernable in 3-6 week old mutants. No abnormalities were detected in the ERG signal obtained in photopic conditions or in the dark adaptation dynamics. The mutants displayed no histologic evidence of retinal degeneration. Retinal output, as measured by visual evoked potentials, was not different from heterozygous control mice. AC1-dependent pathways contribute to the generation of the retinal response to light. They may be necessary for the maintenance of the neural generators of the ERG OP.