Cytosolic calcium transient increase through the AMPA/kainate receptor in cultured Müller cells.

The intracellular concentration of free calcium ions ([Ca2+]i) following administration of glutamate agonist was monitored for retinal Müller cells cultured from adult rabbits using a fluorescence microscope equipped with a video camera system. The calcium concentration was imaged with fura-2. The transient increase of [Ca2+]i was observed following the administration of L-glutamate (3 mM), kainate (0.07-7 mM) and L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA, 0.07-7 mM), but not N-methyl-L-aspartate (NMDA, 0.7-7 mM) in Mg(2+)-free medium. The AMPA/kainate-induced increase of [Ca2+]i was blocked by the non-NMDA glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or low concentrations of external calcium. High K+ solution induced a slight but definite increase in [Ca2+]i which was blocked by nifedipine, a voltage-dependent calcium channel blocker, at 100 microM, suggesting that L-type calcium channels are present in cultured Müller cells. The AMPA-induced transient increase of [Ca2+]i was not blocked at the same concentration of nifedipine. There must be an influx of calcium ions through non-NMDA AMPA-kainate receptors in Müller cells. In the retina, glutamate receptor-linked events are no longer considered as specific to neurons.