Analysis of the light-sensitivity of the photoreceptor cells of the ataxia and male sterility (AMS) mouse, an Nna1 mutant
Article first published online: 9 OCT 2012
© 2012 The Authors. Pathology International © 2012 Japanese Society of Pathology and Wiley Publishing Asia Pty Ltd
Volume 62, Issue 11, pages 719–727, November 2012
How to Cite
Araki, A., Maruyama, R., Harada, Y., Ishikawa, N. and Harada, T. (2012), Analysis of the light-sensitivity of the photoreceptor cells of the ataxia and male sterility (AMS) mouse, an Nna1 mutant. Pathology International, 62: 719–727. doi: 10.1111/j.1440-1827.2012.02861.x
- Issue published online: 1 NOV 2012
- Article first published online: 9 OCT 2012
- Received 10 June 2012. Accepted for publication 13 September 2012.
- Nna1 gene;
- retinal degeneration
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.