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A. Bringmann, O. Uckermann, T. Pannicke, I. Iandiev, B. Biedermann, A. Reichenbach, P. Wiedemann; Dopamine–Mediated Volume Regulation of Glial Cells in the Rat Retina . Invest. Ophthalmol. Vis. Sci. 2004;45(13):5292.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose:Beside extracellular fluid accumulation, the swelling of glial cells represents a hallmark of edema development in the retina. The cysts which develop during cystoid macular edema were suggested to represent swollen and dying glial (Müller) cells (Yanoff et al., Surv. Ophthalmol. 28  S505–S511). Ischemic–hypoxic conditions have been crucially implicated in the development of retinal edema. However, the cellular mechanisms underlying glial cell swelling are poorly understood. Recently, we proposed a mechanism of post–ischemic glial cell swelling where downregulation of their K+ conductance prevents the emission of intracellularly accumulated K+ ions, resulting in osmotically driven water fluxes from the blood into the glial cells via aquaporins (AQPs). In the present study, we investigated the effect of dopamine on glial cell swelling. Dopamine, acting at D2 receptors, has been described to inhibit K+ currents in Müller cells (Biedermann et al., Neuroreport 6  609–612), as well as water fluxes through AQP4 (Zelenina et al., Am. J. Physiol. 283  F309–F318). Methods:Transient retinal ischemia was induced in one eye of adult rats by elevating the intraocular pressure for 60 min. Three days after ischemia, the alteration of the cross–sectional area of Müller cell somata upon hypotonic stress (a situation resembling hypoxia–induced cytotoxic edema in the brain) was recorded in acutely isolated retinal slices. Results: We found that control cells did not swell under hypotonic condition; however, significant swelling was induced after preincubation of dopamine or of a D1 receptor agonist. Cells from postischemic retinas swell upon hypotonic stress; preincubation of dopamine inhibited this response. The effect of dopamine is suggested to be mediated by activation of D2 receptors, since a selective D2 receptor agonist significantly reversed the cell swelling in postischemic retinas, while a D1 receptor agonist was largely ineffective. Conclusions: It is suggested that, under normal conditions, D1 receptor stimulation may favor glial cell swelling, via closure of K+ channels. In postischemic retinas where the glial cells display a downregulated K+ conductance, D2 receptor stimulation results in inhibition of cell swelling, likely via blockage of water fluxes through AQP4.
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