Cited by 23Retinal Development and DisordersRetinal Diseases and TreatmentsGenetics, Aging, and Longevity in Model Organisms

A morphological and morphometrical study of the retina in aging SAM mice

Shoji, Masato, Okada, Morio, Ohta, Akira, Higuchi, Keiichi, Hosokawa, Masanori, Honda, Yoshihito·1998·Ophthalmic Research

Abstract

We investigated whether neuronal cell loss occurred as a part of normal aging of the retina in the Senescence-Accelerated Mouse, strains SAMP1 and SAMR1, and in the BALB/c mouse. All three strains showed age-related atrophy of the retina after histologically normal development. Morphometrical study revealed the following facts. The rate of loss of photoreceptor cells in the peripheral retina was greater than in the central retina in all three strains. In the central retina, the rate of loss of photoreceptor cells was greater in the SAMP1 and SAMR1 mice than in the BALB/c mice. In the peripheral retinal, the SAMR1 and SAMP1 strains had fewer cells than the BALB/c strain at all ages, but the rate of loss of these cells did not differ among the three strains. The rate of loss of ganglion cells did not differ between the peripheral and central retinas in the three strains. The SAMR1 and SAMP1 strains had fewer ganglion cells in the peripheral retina than the BALB/c strain at all ages. Because the rate of age-related loss of these cells in SAMP1 mice was not accelerated, and they were short-lived, SAMP1 mice did not show marked age-related loss. On the contrary, the SAMR1 mice showed a marked loss of photoreceptor cells and ganglion cells late in life because of their longer life span, and we propose that this strain is a suitable animal model for the study of mechanisms of age-related loss of neuronal cells in the retina.

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Crossref · 10.1159/000055471

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  • By 25 months of age, SAMR1 mice had near complete loss of the photoreceptor layer peripherally and significant loss of the photoreceptor and ganglion cells centrally.

    “By 25 months of age, SAMR1 mice had near complete loss of the photoreceptor layer peripherally and significant loss of the photoreceptor and ganglion cells centrally”

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References 31 · Cited by 23

Authors
Shoji, M., Okada, M., Ohta, A., Higuchi, K., Hosokawa, M., & Honda, Y.
Affiliations
Kyoto University (JP)
Venue
Ophthalmic Research
Publisher
S. Karger AG
Published
1998
Volume
30
Issue
3
Pages
172-179
ISSN
  • 0030-3747 (ISSN-L)
  • 1423-0259
OpenAlex
W1987588502
Cited by
23
References
31
Citations by year
2022: 2 · 2013: 1 · 2012: 3
FWCI
0.70
Type
journal article
Language
en
Open access
closed
Locations
  • Ophthalmic Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
  • Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords
retinal aging, photoreceptor loss, retinal ganglion cells, neuronal loss, senescence-accelerated mice, SAMP1, SAMR1, BALB/c mice, peripheral retina, central retina
MeSH terms
Aging, Animals, Atrophy, Cell Count, Disease Models, Animal, Mice, Inbred BALB C, Mice, Mutant Strains, Photoreceptor Cells, Retina, Retinal Ganglion Cells, Mice

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