Vitellogenic oocytes and eggs of the frog Xenopus laevis contain intermediate-size filaments that are resistant to extractions in high-salt buffers and Triton X-100 and are specifically stained with antibodies to cytokeratins. Gel electrophoresis of cytoskeletal proteins from Xenopus oocytes shows a specific enrichment of three polypeptides designated components 1 [Mr, 56,
We tested the optokinetic nystagmus (OKN) reflex of various hypopigmented mutant mice and ultrastructurally examined the pigmentation of various ocular structures in these mutants. Using electron microscopy we examined the pigmentation of the choroid and retinal pigment epithelium (RPE) and measured the numerical density, volume density, and distribution of RPE melanosomes of mice with the following phenotypes: (1) wild type, (2) mutants that have abnormal or no OKN in response to horizontally moving, full-field stimulation, and (3) other mutants that have normal OKN but reduced choroidal pigmentation. We also measured the OKN of all these mice in response to horizontally moving stimuli that were restricted to the nasal or to the temporal retina. We found that in the mutants with normal OKN the numerical density of melanosomes in the RPE was within the range found for wild type, while the numerical density was reduced for the mutants with abnormal OKN. For one mutant with normal RPE pigmentation and normal OKN, the choroidal pigmentation was nearly absent. For the genotypes with abnormal OKN the volume density of the RPE melanosomes and percent apical melanosomes were sometimes greater and sometimes less than normal. The OKN patterns of these mice fell into the following categories: (1) wild type; (2) field-restriction dependent OKN with small following movements but no OKN in response to full-field stimulation, normal OKN in response to stimulation of the nasal retina, and OKN of reversed direction in response to stimulation of the temporal retina; (3) oblique with slow oblique following movements and reduced numbers of OKNs with oblique quick phases in response to horizontally moving, full-field stimulation, nearly normal OKN in response to stimulation of the nasal retina, and OKN of reversed direction in response to stimulation of the temporal retina. The horizontal component of the oblique response to full-field stimulation was in the same direction for the two eyes, but the vertical component was in the opposite direction. (4) Slow, small amplitude, with no or very small following movements in response to full-field stimulation, following movements in response to stimulation of the nasal retina and reversed "following" movements in response to stimulation of the temporal retina but few or no quick phases of the OKN for any stimulus condition. These results show that a variety of abnormalities of the OKN occur for hypopigmentation mutants of the mouse.(ABSTRACT TRUNCATED AT 400 WORDS)
The time of maximal occurrence of pyknotic nuclei in the retinal ganglion cell layer of postnatal pearl mutant mice is earlier than that in normal mice (Linden and Pinto 1985). Both ganglion and displaced amacrine cells and glia populate the ganglion cell layer. Thus, in order to show that ganglion cells themselves are affected, we counted the numbers of surviving axons in the optic nerve of postnatal day (PND) 0, 4, 12 and adult mice. On PND 0, pearl mutant mice had 139,000 +/- 2800 (SEM) optic axons, about 8% more than wild-type mice (128,000 +/- 1,700; p = 0.031) but on PND 4, pearl mutants had 24% fewer axons than wild-type mice (96,000 +/- 3700 and 119,000 +/- 4600, respectively; p = 0.008). Thus, pearl mutants lose nearly five times as many retinal ganglion cells as wild-type mice in the interval from PND 0 to 4. The number of axons present in adult mice was nearly equal (56,700 +/- 3200 for wild-type and 52,500 +/- 2700 for pearl mutants p = 0.37). We searched for evidence for changes in the schedule of cell death among other neurons of the retina by counting the number of pyknotic nuclei in the various retinal layers. On PND 4, pearl mutant mice had more pyknotic nuclei in the neuroblastic layer than wild-type mice (5000 +/- 400 and 3900 +/- 300, respectively; p less than 0.05). The time-course of the appearance of pyknotic nuclei in the outer nuclear layer differed for the two genotypes (ANOVA, F = 12.5, p less than 0.001). The most striking difference was a greater number of pyknotic nuclei on PND 20 for the pearl mutants (1300) than for wild-type (480; p = 0.002). However, the total number of photoreceptors in adults did not differ between the two genotypes (3.6 x 10(6) +/- 2.4 x 10(5) for wild-type and 3.7 x 10(6) +/- 3.3 x 10(5) for pearl; p greater than 0.8). These results, taken together, show that natural cell death occurs at an earlier time for retinal ganglion cells of pearl mutants, but that the total number of retinal neurons surviving to adulthood is not affected appreciably by the mutation.
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