December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Diabetic Changes in Retinal Electrophysiology
Author Affiliations & Notes
  • HA Hancock
    UAB Birmingham AL
  • BD Gerwin
    UAB Birmingham AL
  • DE Allen
    Physiological Optics
    UAB Birmingham AL
  • RH Kramer
    Molecular Biology UC Berkeley Berkeley CA
  • TW Kraft
    Physiological Optics
    UAB Birmingham AL
  • Footnotes
    Commercial Relationships   H.A. Hancock, None; B.D. Gerwin, None; D.E. Allen, None; R.H. Kramer, None; T.W. Kraft, None. Grant Identification: NIH EY10573 (TWK) and EY12608 (RHK)
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 1347. doi:
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      HA Hancock, BD Gerwin, DE Allen, RH Kramer, TW Kraft; Diabetic Changes in Retinal Electrophysiology . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1347.

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

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Abstract: : Purpose: Diabetic retinopathy is the leading cause of new blindness in adults 21 to 75 years old. We sought to induce diabetic changes in the retina, using the ERG to monitor suspected pathological changes. We then wanted to observe the photoreceptor component of the ERG, in vivo and in isolation to determine if any of the diabetic changes in retinal electrophysiology had photoreceptor components and/or origins. Methods: The development of electroretinographic changes was followed for up to six weeks in experimental rats with streptozotocin-induced diabetes and in control animals. Using an Ussing chamber and the isolated retina, we then compared the massed photoresponse in diabetic and control tissues, and finally looked at the effects of IGF-1 on tissues from normal and diabetic animals. Results: The changes in the photoresponse of the diabetic animals was variable and most profound in the animal with the most significant ERG changes. There was as much as a four-fold decrease in sensitivity and a change in the waveform of the response resulting in an early peak followed by a plateau prior to recovery. As previously published, IGF-1 increased the response amplitude and accelerated the peak time and recovery of the control photoresponse; the diabetic tissue showed little, if any response to the presence of IGF-1.The peak latencies of the a- and b- waves of the ERG did not differ significantly in the diabetic and control rats. However, oscillatory potential (OP) peaks were found to be delayed in diabetic rats several weeks after streptozotocin treatment. No attempt was made to control the blood sugars of the diabetic animals; fasting blood sugar was over 500 mg/dL at the time of sacrifice. There was also significant weight loss in these animals. Conclusion: Chemically induced diabetic changes in blood glucose can lead to delays in the oscillatory potentials as described by Sakai et al. 1995. Dramatic changes in the massed photoreceptor responses was noted at this time, and may precede changes in the oscillatory potentials.

Keywords: 517 photoreceptors • 388 diabetic retinopathy • 555 retina: distal(photoreceptors, horizontal cells, bipolar cells) 

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