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Analysis of the light‐sensitivity of the photoreceptor cells of the ataxia and male sterility (AMS) mouse, an Nna1 mutant
Author(s) -
Araki Asuka,
Maruyama Riruke,
Harada Yuji,
Ishikawa Noriyoshi,
Harada Takayuki
Publication year - 2012
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/j.1440-1827.2012.02861.x
Subject(s) - atrophy , outer nuclear layer , retina , retinal degeneration , biology , stimulation , programmed cell death , retinal , sterility , mutant , photoreceptor cell , ataxia , microbiology and biotechnology , pathology , endocrinology , neuroscience , medicine , genetics , gene , apoptosis , biochemistry
We confirmed retinal degeneration in the ataxia and male sterility (AMS) mouse, a mutant of the Nna1 gene, and examined the photosensitivity of the photoreceptors to determine how closely related the intrinsic and extrinsic factors were in triggering photoreceptor cell death. The AMS mice reared in a dark environment did not show atrophy of the outer nuclear layer (ONL) before 4 weeks of age, but in the older mice, retinal atrophy progressed in the same manner as in the AMS mice housed under normal light conditions. Examining the sensitivity to intentional light stimulation revealed the atrophy of the AMS retina to be exacerbated by a weak light. After administering strong light irradiation, equally severe ONL atrophy occurred in both the wild‐type and AMS mice. These results indicate that in addition to functional loss of Nna1, another injurious stimulation is necessary to trigger death signals in photoreceptor cells during the postnatal period, but the cells die gradually and autonomously in older age, and that the mutation makes the cells vulnerable to a weak light, but does not increase the number of cells sensitive to strong light stimulation. Thus, these two factors are mutually independent death triggers in AMS photoreceptor cells.