April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
The Senescence-Accelerated Mouse in Retinal Neurodegeneration
Author Affiliations & Notes
  • Yasunari Munemasa
    Ophthalmology, St Marianna University, Kawasaki, Japan
  • Yasushi Kitaoka
    Ophthalmology, St Marianna University, Kawasaki, Japan
  • Kaori Kojima
    Ophthalmology, St Marianna University, Kawasaki, Japan
  • Junko Kuribayashi
    Ophthalmology, St Marianna University, Kawasaki, Japan
  • Satoki Ueno
    Ophthalmology, St Marianna University, Kawasaki, Japan
  • Footnotes
    Commercial Relationships  Yasunari Munemasa, None; Yasushi Kitaoka, None; Kaori Kojima, None; Junko Kuribayashi, None; Satoki Ueno, None
  • Footnotes
    Support  This work was supported by Grants-in Aid for Scientific Research No.21791718(Y.M.) and No.22659315 (Y.K.); Uehara Memorial Foundation (Y.M.)
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 4679. doi:
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      Yasunari Munemasa, Yasushi Kitaoka, Kaori Kojima, Junko Kuribayashi, Satoki Ueno; The Senescence-Accelerated Mouse in Retinal Neurodegeneration. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4679.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : The senescence-accelerated mouse (SAM) has been established as a model of accelerated aging. SAM consists of the senescence-accelerated prone mouse (SAMP) and senescence-accelerated resistant mouse (SAMR). SAMP shows a shortened life span and early manifestations of senescence, while SAMR shows normal aging characteristics. In the SAMP series, SAMP8 and SAMP10 shows dysfunction of learning and memory and brain atrophy through several molecular pathways, such as PI3K/Akt, NOS, and amyloid precursor protein (APP)/amyloid beta. In the present study, we investigated the difference of retinal neurodegeneration in SAMR and SAMP using optic nerve crush (ONC) model.

Methods: : Six month male SAMR, SAMP8, and SAMP10 were used in this study. To generate ONC, the nerve of one eye was exposed and clamped approximately 0.5 mm from the globe with self-closing forceps for 10 s, contralateral eye was used as a control. The eyes were enucleated at 2 weeks after ONC. Morphological analysis was performed with whole mount retinas stained with 1% cresyl violet. The number of neural cells in the retinal ganglion cell layer (RGCL) was counted at two fields in each retinal quadrant with light microscope and care was taken to ensure that the fields were the same distance from the center of the optic nerve.

Results: : The neural cells number in the RGCL was expressed as % of contralateral control. The number of neural cells in the RGCL of SAMR retina showed 63.8 ± 3.5% at 2 weeks after ONC, compared with the contralateral control. The neural cells number of SAMP8 and SAMP10 were 73.8 ± 5.8 % and 45.5 % ± 1.9 %, respectively. The number of neural cells in SAMP10 was significantly decreased after ONC, compared with those after ONC in SAMR, whereas no significant change in SAMP8 was observed, compared with SAMR.

Conclusions: : The neural cell in the RGCL of SAMP10 retina was more vulnerable than SAMR control, which exhibits normal aging process, against ONC. This result suggested the involvement of SAMP10 senescence in retinal neurodegeneration.

Keywords: retinal degenerations: cell biology • aging • optic nerve 

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