PubMed1981
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.