Purpose. We have previously demonstrated that the metabotropic glutamate receptor agonist ACPD evokes an increase in intracellular calcium concentration ([Ca2+]i) in isolated retinal Müller cells (Keirstead and Miller, 1992, Soc. Neurosci. Abstr. 18:1030). In the present study we have further characterized neurotransmitters that can modulate [Ca2+]i in Müller cells. Methods. Müller cells were isolated from larval tiger salamander retinas and [Ca2+]i was measured in using the calcium indicator Fura-2 and digital video fluorescence microscopy. Results. Bath application of glutamate (30-50 μM), quisqualate (10-50 μM) and L-AP4 (5-100 μM) evoked an increase in [Ca2+]i in Müller cells in the absence of extracellular Ca2+. The neuoractive peptide, bradykinin (1.0-5.0 μM), also evoked a similar release of Ca2+ from intracellular stores. The Ca2+ release triggered by these compounds often occurred first in the distal end of the cell, and later or not at all in the endfoot of these elongated cells. In addition, bath application of ATP (1-100 μM) in calcium-free medium evoked a steep increase in [Ca2+]i that was reversibly inhibited by the nonspecific purinergic receptor antagonist, suramin (0.1-1.0 mM). This suggests that the ATP-evoked release was mediated by a G-protein coupled purinergic receptor. Conclusion. Müller cells possess a variety of metabotropic receptors that are coupled to Ca2+ release mechanisms. Consequently, changes in neuronal activity can have a dynamic effect on glial cell physiology, which in turn can affect retinal homeostasis.
|Original language||English (US)|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Feb 15 1996|