Neuropharmacology and NeurotoxicologyATP induces Ca2+ release from IP3-sensitive Ca2+ stores exclusively in large DRG neuronesSvichar, Natalia1; Shmigol, Anatoly1; Verkhratsky, Alexej2,3; Kostyuk, Platon1Author Information 1Bogomoletz Institute of Physiology and International Center of Molecular Physiology, Bogomoletz St. 4, Kiev-24, GSP 252601, Ukraine. 2Present Address: Max-Delbrück Center for Molecular Medicine, Robert-Rössle Strasse 10, 13122 Berlin-Buch, Germany 3Corresponding Author and Address: Alexej Verkhratsky, Max-Delbrück Center for Molecular Medicine, Robert-Rössle Strasse 10, 13122 Berlin-Buch, Germany ACKNOWLEDGEMENTS: This research was supported in part by INTAS (International association for the Promotion of the Cooperation with Scientists from the New Independent States of the former Soviet Union) grant to P.K. and by Wellcome Trust Collaborative Research Grant to A.V. The authors thank Ludmila Grigorovitch for excellent technical assistance. Received 28 January 1997; accepted 6 March 1997 NeuroReport: May 6, 1997 - Volume 8 - Issue 7 - p 1555-1559 Buy Abstract PURINORECEPTOR-MEDIATED intracellular Ca2+ release was studied in freshly isolated adult mouse dorsal root ganglia (DRG) neurones. The cytoplasmic Ca2+ concentration ([Ca2+]i) was measured using indo-1-based microfluorimetry. The application of 100 μM ATP in Ca2+-free solution triggered an increase in [Ca2+]i in 93% of large DRG neurones but in no small ones. The ATP-induced [Ca2+]i transients in large neurones were inhibited by cells incubation with thapsigargin or by intracellular dialysis with heparin-containing solution. The ATP-triggered increase in [Ca2+]i was not mimicked by adenosine and was blocked by suramin, suggesting the involvement of metabotropic (P2Y) purinoreceptors. We conclude that large (proprioceptive) DRG neurones express P2Y purinoreceptors linked to the inositol 1,4,5-triphosphate-Ca2+ intracellular signal transduction cascade, whereas small (nociceptive) DRG neurones are devoid of such a mechanism. © Lippincott-Raven Publishers.