Purchase this article with an account.
M. Wang, D.M. Sherry, J.G. Robson, L.J. Frishman; Expression of Inward Rectifying Potassium Channels Kir4.1 and Kir2.1 in the Mouse Retina and Their Roles in Generating the Scotopic ERG . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4730.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To investigate the role of Kir4.1 and Kir2.1 channels in generating the scotopic ERG and to compare the distribution of these channels in adult wildtype (Kir +/+) mice (C57/BL6), and in transgenic mice hemizygous for Kir4.1.
Scotopic ERGs were recorded monocularly from anesthetized adult control C57/BL6 mice, Kir4.1 hemizygous (+/–) mice and wildtype (WT) littermates. Hemizygous mice were used because Kir4.1(–/–) mice survive less than a month after birth. In some control mice, ERGs also were recorded after intravitreal injection of barium (1– 2 mM) to block Kir channels. From the weakest intensity up to those for which a–waves appeared, amplitudes measured near the peaks of the b–wave (110 ms after the flash) and the negative scotopic threshold response (nSTR; 200 ms) were fit with a previously developed model of the scotopic ERG in C57/BL6 mice. The model included 5 components: photoreceptor (PIII), rod bipolar cell (PII), nSTR, positive STR (pSTR) and a positive scotopic (pSR) response. After recording, the mice were euthanized and the eyes were prepared for immunolabeling. Retinal cryosections were labeled for Kir4.1 or Kir2.1. To assess Kir 4.1 and 2.1 localization in Müller cells specifically, sections were double labeled for glutamine synthetase. Labeling was visualized by confocal microscopy.
A–waves– and maximum b–wave amplitudes of the scotopic ERG were similar in all mice. However, the most sensitive positive potentials (pSTR and pSR, up to 10% percent of the b–wave) were absent in Kir(+/–) mice. For the Kir4.1 (+/–) mice, only three model components, PIII, PII and the nSTR were necessary to fit the data measured at 110 ms and 200 ms. As previously demonstrated in other species, the nSTR was eliminated by barium indicating a Müller–cell origin for the response. In control mice, Kir4.1 was concentrated in Müller–cell end feet and around the blood vessels. In Kir4.1 (+/–) mice, Kir4.1 immunolabeling was weaker than control in the end feet, and much less obvious around blood vessels. The Kir2.1 immunoreactivity in Kir4.1 (+/–) mice was similar to that in controls, located predominantly in Müller–cell lateral processes, around somas and along stem processes.
Our results indicate that Kir4.1 channels in Müller cells play a critical role in generating the sensitive positive components, but not the nSTR of the mouse scotopic ERG. However, Kir2.1 (or other Kir channels) are probably involved in the generation of the nSTR.
This PDF is available to Subscribers Only