Expression of voltage-activated potassium KCNQ channels in mouse eye

BARILA, E.P.; GERMAN, O.L.; CARIGNANO, C.; SPITZMAUL, G.

Buenos Aires

Congreso; 2nd FALAN Congress 2016; 2016

Federation of Latin American and Caribbean Neuroscience Societies

KCNQ channels (Kv7) are voltage-gated K+ channels with 5 members in mammals (KCNQ1-5). In SNC they generate the M-current that regulates neuronal excitability. Also, they provide K+ currents in other tissues, such as cochlea, intestine and smooth muscle. Mutations in 4 of the 5 subunits produce human genetic diseases, such as cardiac arrhythmia (KCNQ1), neonatal epilepsy (KCNQ2 and KCNQ3), and progressive hearing loss (KCNQ4). Others have reported the expression of KCNQ4 and -5 in the retina where it may participate in the visual processing. Our aim was to investigate the expression and function of KCNQ4 and -5 channels in the eye using KO mice for each channel. Using KO-controlled immunohistochemistry, we found a weak labeling of KCNQ4 in retinal pigmented epithelium (RPE) cells, which is enhanced in albino mice. Also, KCNQ4 signal was stronger in pigmented epithelium cells (PE) of the ciliary body. KCNQ5 was found neither in the retina nor in RPE or PE cells. A non-specific signal for KCNQ5 was observed in both genotypes (WT and Kcnq5-/-) under normal staining and it was lost in the retina after antigen retrieval. The signal remained in vestibular organ of WT (control tissue). Patch-clamp analysis on retinal slices of WT mice showed a K+ current insensitive to the channel blocker XE991, while in RPE cells, K+ currents were slightly sensitive to the blocker. Our results indicate that KCNQ4 may participate in the homeostasis of K+ in the subretinal space and ciliary body.