May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Near–Infrared Light Therapy for Retinitis Pigmentosa
Author Affiliations & Notes
  • J.T. Eells
    Health Sciences, University of Wisconsin–Milwaukee, Milwaukee, WI
  • D.K. Kirk
    ACR Center for Vision Sciences, Research School of Biological Sciences, The Australian National University, Canberra, Australia
  • J. Cribb
    ACR Center for Vision Sciences, Research School of Biological Sciences, The Australian National University, Canberra, Australia
  • K. Valter
    ACR Center for Vision Sciences, Research School of Biological Sciences, The Australian National University, Canberra, Australia
  • K.D. DeSmet, V
    Health Sciences, University of Wisconsin–Milwaukee, Milwaukee, WI
  • J.N. VerHoeve
    Ophthalmology, University of Wisconsin, Madison, WI
  • H.T. Whelan
    Neurology, Medical College of Wisconsin, Milwaukee, WI
  • J. Stone
    ACR Center for Vision Sciences, Research School of Biological Sciences, The Australian National University, Canberra, Australia
  • Footnotes
    Commercial Relationships  J.T. Eells, None; D.K. Kirk, None; J. Cribb, None; K. Valter, None; K.D. DeSmet, None; J.N. VerHoeve, None; H.T. Whelan, None; J. Stone, None.
  • Footnotes
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Investigative Ophthalmology & Visual Science May 2006, Vol.47, 1022. doi:
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      J.T. Eells, D.K. Kirk, J. Cribb, K. Valter, K.D. DeSmet, V, J.N. VerHoeve, H.T. Whelan, J. Stone; Near–Infrared Light Therapy for Retinitis Pigmentosa . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1022.

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

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Abstract

Purpose: : Near–infrared (NIR) light–emitting diode (LED) arrays have been shown to stimulate mitochondrial respiration and improve functional recovery of the retina and optic nerve after acute toxic injury. The present study was undertaken to test the hypothesis that a brief course of 670 nm LED treatment would improve mitochondrial function, attenuate oxidative stress and improve photoreceptor survival in a rodent model of retinitis pigmentosa, the P23H rat.

Methods: : Normal SD and P23H rat pups were exposed to 4 joules cm2 of 670 nm light from a light emitting diode (LED) array or received sham treatment once per day for 5 days from postnatal day (pnd) 16 to 20. At pnd 21, retinae were collected and mitochondrial metabolism was assessed by measurement of cytochrome oxidase activity. The other eye of each animal was immersion fixed in 4% paraformaldehyde, washed, cryoprotected in 15% sucrose and sectioned at 14 microns. TUNEL labeling was performed to detect apoptotic cells.

Results: : In both P23H and SD rats, 670 nm LED treatment increased cytochrome oxidase activity when compared to untreated littermate controls. Treatment with 670 nm light attenuated photoreceptor death by nearly 50% in the P23H rat compared with untreated littermate controls. In SD rats, 670 nm light treatment produced a small, but statistically significant, increase in photoreceptor cell death compared with littermate controls.

Conclusions: : Excess photoreceptor degeneration in the P23H retinal begins just after eye opening, peaks in early postnatal life then slows, but persists into adulthood. Previous studies in our laboratory have demonstrated the neuroprotective and retinoprotective actions of 670 nm light treatment in vitro and in vivo. The present study extends these findings to include protection against photoreceptor degeneration in P23H rats. The results of these studies further support the use of 670 nm light therapy in the treatment of retinal injury and degenerative retinal disease

Keywords: retinal degenerations: hereditary • mitochondria • photoreceptors 
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