Purchase this article with an account.
A. V. Chappelow, J. Wu, N. S. Peachey; P2Y2 Receptor Deficient Mice Generate an Electroretinographic Light Peak. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2846. doi: https://doi.org/.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To evaluate the hypothesis that Ca2+ release by the P2Y2 purinergic receptor (P2Y2R; localized to the retinal pigment epithelium (RPE) apical membrane) in response to an increase in ATP initiates the light peak (LP) of the electroretinogram (ERG). P2Y2 receptor deficient (P2Y2R-/-) mice have been generated to study Ca2+ signaling in the lung; however, electrophysiological responses from the retina and RPE of these mice have not been reported to date.
We recorded ERG responses from P2Y2R-/- mice and age-matched control mice following overnight dark adaptation and pupillary dilation. Strobe flash stimuli were used to evaluate photoreceptor and inner retinal function. Long (7 minute) duration stimuli were used to evaluate response components generated by the RPE. Intensity response functions were generated for both stimulus conditions.
Electroretinographic responses of P2Y2R-/- mice appeared comparable to those of control animals under all stimulus conditions examined. Preservation of the ERG a-wave indicated that photoreceptor function was unaltered by the absence of the P2Y2R. All response components generated by the RPE, including the LP, were spared in P2Y2R-/- mice.
Localization of the P2Y2R to the RPE apical membrane suggests a role in LP generation and photoreceptor homeostasis. The maintenance of normal ERG a-waves and LPs in P2Y2R-/- mice indicate that P2Y2R.is not required for preservation of photoreceptors or for initiation of the LP.
This PDF is available to Subscribers Only