Rapid transient changes in axial transmission of near infrared light through the outer segments of retinal rods of Bufo marinus are induced by illumination. The reasons for these changes are not clear. The changes in optical transmission may be useful in the study of photoreceptor function. However, the study of photoreceptor functions through the use of indicator dyes may be confounded by the intrinsic light-induced changes of optical properties of the photoreceptor cells.

Mice of the mutant strain pearl (pe/pe) differ from the wild strain by a single gene mutation, which leads to a lightening of the coat color. We tested this strain to see if this mutant gene also expressed itself in one or more visual abnormalities. Pearl mice were found to lack totally the optokinetic nystagmus reflex that was present in every normal mouse that we examined. This lack of optokinetic nystagmus was not due to oculomotor defects, since postrotatory nystagmus was normal. As described for other pigmentation mutants, we found that pearl mutants had a reduced ipsilateral projection to the lateral geniculate nucleus, superior colliculus, and visual cortex. We recorded from single cells in the superior colliculus and found response properties and light sensitivities to be normal over the luminance range at which optokinetic nystagmus was tested. However, at very dim backgrounds (scotopic levels), the incremental sensitivities of these cells in pearl mice were about 100 times lower than those of normal mice. This reduction in sensitivity was restricted to scotopic backgrounds and was not due to abnormalities in either the time course of dark adaptation or the receptive field sizes of single cells. In recordings of the electroretinographic response, both the waveforms and the normalized magnitudes of the A and B waves of pearl were indistinguishable from those of normal mice, which seems to indicate that the cause of pearl's sensitivity defect is located central to the main electrical events in the photoreceptors. The normality of many aspects of the visual system of pearl mice contrasts sharply with the complete absence of optokinetic nystagmus, with the reduced ipsilateral projection, and with the reduced dark sensitivity of the cells in the superior colliculus.

Intracellular recordings were made from axon bearing horizontal cells in isolated retinas (with retinal pigment epithelium removed) of normal and pearl mutant mice superfused with mammalian Ringer's solution. Cells were injected with Lucifer yellow and identified by their morphology and their response wave-forms. On impalement, we measured a dark, resting voltage of 25-35 mV. All cells had similar spectral sensitivities that were consistent with the CIE scotopic relative spectral luminosity function. For stimuli of high irradiance, two types of responses could be distinguished, based on their waveform at stimulus offset. One consisted of a rapid and wavelength-dependent repolarization followed by a small, slow hyperpolarization. The other consisted of a large, long-lived, and wavelength-independent after-hyperpolarization. The former were recorded from the somatic end and the latter from the axon terminal arborization. The spatial distribution of sensitivity was measured in over 100 locations within the receptive field using small stimuli. The area within which sensitivity of the soma was within 0.1 log unit of the maximal sensitivity was larger than that of the soma dendritic field, but the sizes were nearly equal for the terminal arborization. No secondary maximum of sensitivity was noted over the dendritic field of the unimpaled part of the cell. For the terminal arborization, the half-saturating irradiance for diffuse 502 nm stimuli was about 180 photons micron-2 sec-1, about one-tenth that for the soma. These values are in good agreement with those for cat and rabbit.(ABSTRACT TRUNCATED AT 250 WORDS)