KCNQ5/K(v)7.5 potassium channel expression and subcellular localization in primate retinal pigment epithelium and neural retina

Department of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI 48105, USA.
AJP Cell Physiology (Impact Factor: 3.78). 07/2011; 301(5):C1017-26. DOI: 10.1152/ajpcell.00185.2011
Source: PubMed


Previous studies identified in retinal pigment epithelial (RPE) cells an M-type K(+) current, which in many other cell types is mediated by channels encoded by KCNQ genes. The aim of this study was to assess the expression of KCNQ genes in the monkey RPE and neural retina. Application of the specific KCNQ channel blocker XE991 eliminated the M-type current in freshly isolated monkey RPE cells, indicating that KCNQ subunits contribute to the underlying channels. RT-PCR analysis revealed the expression of KCNQ1, KCNQ4, and KCNQ5 transcripts in the RPE and all five KCNQ transcripts in the neural retina. At the protein level, KCNQ5 was detected in the RPE, whereas both KCNQ4 and KCNQ5 were found in neural retina. In situ hybridization in frozen monkey retinal sections revealed KCNQ5 gene expression in the ganglion cell layer and the inner and outer nuclear layers of the neural retina, but results in the RPE were inconclusive due to the presence of melanin. Immunohistochemistry revealed KCNQ5 in the inner and outer plexiform layers, in cone and rod photoreceptor inner segments, and near the basal membrane of the RPE. The data suggest that KCNQ5 channels contribute to the RPE basal membrane K(+) conductance and, thus, likely play an important role in active K(+) absorption. The distribution of KCNQ5 in neural retina suggests that these channels may function in the shaping of the photoresponses of cone and rod photoreceptors and the processing of visual information by retinal neurons.

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    • "Recently, the group of Hughes was able to verify the molecular identity of the channel composed of KCNQ4 and KCNQ5 subunits (Pattnaik and Hughes, 2012; Zhang et al., 2011) using RT-PCR, immunohistochemistry and various compounds , including retigabine, N-ethyl-maleimide and diclofenac, to assess the activation and inhibition patterns of the channel. Interestingly , the M-type current in the RPE cannot be activated by increases in the intracellular cAMP (Pattnaik and Hughes, 2012; Zhang et al., 2011). The localization of these channels to the basolateral membrane and their large voltage-range of activity make it very likely that these channels contribute to transepithelial K þ transport by the RPE (Figs. 2 and 3 "
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