Pressure-dependent modulation of inward-rectifying K⁺ channels: implications for cation homeostasis and K⁺ dynamics in glaucoma.

ABSTRACT: Glaucoma is the leading cause of blindness worldwide, resulting from degeneration of retinal ganglion cells (RGCs), which form the optic nerve. Prior to structural degeneration, RGCs exhibit physiological deficits. Müller glia provide homeostatic regulation of ions that supports RGC physiology through a process called K⁺ siphoning. Recent studies suggest that several retinal conditions, including glaucoma, involve changes in the expression of K⁺ channels in Müller glia. To clarify whether glaucoma-related stressors directly alter expression and function of K⁺ channels in Müller glia, we examined changes in the expression of inwardly rectifying K⁺ (Kir) channels and two-pore domain (K2P) channels in response to elevated intraocular pressure (IOP)

SUBMITTER: Fischer RA 

PROVIDER: S-EPMC6732416 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature