March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Erg Changes In A Triple Transgenic Mouse Model For Alzheimer`s Disease
Author Affiliations & Notes
  • Gabriela L. Ioshimoto
    Experimental Psychology, University of Sao Paulo, Sao Paulo, Brazil
    Neuroscience and Behavior, Sao Paulo, Brazil
  • Balazs V. Nagy
    Experimental Psychology, University of Sao Paulo, Sao Paulo, Brazil
    Neuroscience and Behavior, Sao Paulo, Brazil
  • Jan J. Kremers
    Dept of Ophthalmology, University of Erlangen, Erlangen, Germany
    Rhenovia Pharma, Mulhouse, France
  • Dora F. Ventura
    Experimental Psychology, University of Sao Paulo, Sao Paulo, Brazil
    Neuroscience and Behavior, Sao Paulo, Brazil
  • Footnotes
    Commercial Relationships  Gabriela L. Ioshimoto, None; Balazs V. Nagy, None; Jan J. Kremers, None; Dora F. Ventura, None
  • Footnotes
    Support  CAPES
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 5376. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Gabriela L. Ioshimoto, Balazs V. Nagy, Jan J. Kremers, Dora F. Ventura; Erg Changes In A Triple Transgenic Mouse Model For Alzheimer`s Disease. Invest. Ophthalmol. Vis. Sci. 2012;53(14):5376.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: : To study the retinal function of the triple transgenic mouse model (3xTg-AD) for Alzheimer`s disease (AD) by comparing retinal electrophysiological responses in 3xTg-AD mice with those in the background control (b6;129-PS1). The responses were measured between 2 and 12 months of age.

Methods: : ERGs were recorded from 44 3xTg-AD mice and from 23 background controls with a contact lens electrode on the cornea, a needle reference electrode on the head and a ground on the tail. Recordings were obtained for: 1) Maximum scotopic response (30cd.s/m2); 2) Light-adapted (30 cd/m2) flicker pulses (30 cd.s/m2) at 12, 18 and 30 Hz.

Results: : 87% of control mice and 28% of the 3xTg-AD had very abnormal ERGs with a large b-wave implicit time (111,73 ± 22,56 ms) and no OPs. The others displayed ERGs with OPs and with b-wave implicit times within the range (45,31 ± 6,74 ms) expected from the literature. In the latter group, age dependent changes in the flash ERG were found for the a- and b-wave amplitudes. While the control group exhibited a mean decrease from 193,26 to 97,06 μV in the a-wave amplitude and a mean decrease from 452,4 to 230,71 μV in the b-wave amplitude between 6 and 12 months, 3xTg-AD group presented a low and constant response (a-wave= 143,4 ± 19,3 μV; b-wave= 303,5 ± 49,7 μV) between 6 and 12 months of age. Flicker amplitudes (1st harmonic after Fourier analysis) from the 3xTg-AD group were significantly reduced compared to controls at 6 months, but not at 12 months, both for the 12 Hz (p=0,0001) and for the 18 Hz (p=0,0001)stimuli.

Conclusions: : Comparison of control and transgenic mice with ERGs with OPs and implicit times within the normal range, revealed a physiological impairment of the retina of AD mice. The a-wave amplitude decrease suggests that the effect involves loss or impairment of photoreceptor function. We conclude that AD may also affect the function of the retina.

Keywords: electroretinography: non-clinical • pathology: experimental • retina 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×