Calcium Increases in Retinal Glial Cells Evoked by Light-Induced Neuronal Activity

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Abstract
Electrical stimulation of neurons in brain slices evokes increases in cytoplasmic Ca2+ in neighboring astrocytes. The present study tests whether similar neuron-to-glial signaling occurs in the isolated rat retina in response to light stimulation. Results demonstrate that Müller cells, the principal retinal glial cells, generate transient increases in Ca2+ under constant illumination. A flickering light stimulus increases the occurrence of these Ca2+ transients. Antidromic activation of ganglion cell axons also increases the generation of Müller cell Ca2+ transients. The increases in Ca2+ transients evoked by light and antidromic stimulation are blocked by the purinergic antagonist suramin and by TTX. The addition of adenosine greatly potentiates the response to light, with light ON evoking large Ca2+ increases in Müller cells. Suramin, apyrase (an ATP-hydrolyzing enzyme), and TTX substantially reduce the adenosine-potentiated response. NMDA, metabotropic glutamate, GABAB, and muscarinic receptor antagonists, in contrast, are mainly ineffective in blocking the response. Light-evoked Ca2+ responses begin in Müller cell processes within the inner plexiform (synaptic) layer of the retina and then spread into cell endfeet at the inner retinal surface. These results represent the first demonstration that Ca2+ increases in CNS glia can be evoked by a natural stimulus (light flashes). The results suggest that neuron-to-glia signaling in the retina is mediated by neuronal release of ATP, most likely from amacrine and/or ganglion cells, and that the response is augmented under pathological conditions when adenosine levels increase.