Calcium mobilization by muscarinic receptors and ATP receptors during retinogenesis

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Acetylcholine and adenosine triphosphate (ATP) raise intracellular Ca^<2+> concentration via muscarinic receptors and P_<2U> purinoceptors by releasing Ca^<2+> from intracellular Ca^<2+> stores in the neural retina of early embryonic chick. We studied the signal transduction mechanisms for the muscarinic and purinergic Ca^<2+> responses and developmental changes in the purinergic Ca^<2+> responses with fura-2 fluorescence measurements.Pertussis toxin suppressed the ATP-induced Ca^<2+> rise, whereas no inhibition was observed on the muscarinic Ca^<2+> rise. U-73122, an inhibitor of phospholipase C,suppressed the Ca^<2+> rise to ATP,but its analog U-73343 did not suppress it. In contrast, both U-73122 and U-73343 suppressed the muscarinic Ca^<2+> rise. Li^+, which inhibits phosphatidylinositol metabolism, enhanced both the muscarinic and purinergic Ca^<2+> rises. Thapsigargin, an inhibitor of Ca^<2+>-ATPase of inositol trisphosphate (IP_3) -sensitive Ca^<2+> stores, abolished both the muscarinic and purinergic Ca^<2+> rises. Cross-talk occurred between the muscarinic and purinergic Ca^<2+> mobilizations but they were not occlusive. Our study suggests that both the muscarinic and purinergic Ca^<2+> mobilizations utilize IP_3-sensitive Ca^<2+> stores, but different signal transduction pathways are involved in between the muscarinic and purinergic Ca^<2+> responses.The ATP-induced Ca^<2+> rise was the most prominent at E3, drastically declined towards E8 and further decreased until E11-13 before synapse formation. ATP might act as an intercellular messenger during the early period of neurogenesis in the chick retina.