Abstract
Retinal glial (Muller) cells release ATP upon osmotic stress or activation of metabotropic glutamate receptors. ATP inhibits the osmotic Muller cell swelling by activation of P2Y(1) receptors. In the present study, we determined the molecular pathways of the ATP release from Muller cells in slices of the rat retina. Administration of the ATP/ADPase apyrase induced a swelling of Muller cells under ...
Abstract
Retinal glial (Muller) cells release ATP upon osmotic stress or activation of metabotropic glutamate receptors. ATP inhibits the osmotic Muller cell swelling by activation of P2Y(1) receptors. In the present study, we determined the molecular pathways of the ATP release from Muller cells in slices of the rat retina. Administration of the ATP/ADPase apyrase induced a swelling of Muller cells under hypoosmotic conditions, and prevented the swelling-inhibitory effect of glutamate, suggesting that swelling inhibition is mediated by extracellular ATP. A hypoosmotic swelling of Muller cells was also observed in the presence of a blocker of multidrug resistance channels (MK-571), a CFTR inhibitor (glibenclamide), and connexin hemichannel blockers (18-alpha-glycyrrhetinic acid, 100 A mu M carbenoxolone). The swelling-inhibitory effect of glutamate was prevented by MK-571, the connexin hemichannel blockers, and a pannexin-1 hemichannel blocker (5 A mu M carbenoxolone). The p-glycoprotein blocker verapamil had no effect. As revealed by single-cell RT-PCR, subpopulations of Muller cells expressed mRNAs for pannexin-1 and -2, and connexins 30, 30.3, 32, 43, 45, and 46. The data may suggest that rat Muller cells release ATP by multidrug resistance channels, CFTR, and connexin hemichannels in response to osmotic stress, while glutamate induces a release of ATP via multidrug resistance channels, connexin hemichannels, and pannexin-1.
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