Tags

Type your tag names separated by a space and hit enter

ATP increases intracellular calcium in supraoptic neurons by activation of both P2X and P2Y purinergic receptors.
Am J Physiol Regul Integr Comp Physiol. 2007 Jan; 292(1):R423-31.AJ

Abstract

ATP increases intracellular calcium concentration ([Ca(2+)](i)) in supraoptic nucleus (SON) neurons in hypothalamo-neurohypophyseal system explants loaded with the Ca(2+)-sensitive dye, fura 2-AM. Involvement of P2X purinergic receptors (P2XR) in this response was anticipated, because ATP stimulation of vasopressin release from hypothalamo-neurohypophyseal system explants required activation of P2XRs, and activation of P2XRs induced an increase in [Ca(2+)](i) in dissociated SON neurons. However, the ATP-induced increase in [Ca(2+)](i) persisted after removal of Ca(2+) from the perifusate ([Ca(2+)](o)). This suggested involvement of P2Y purinergic receptors (P2YR), because P2YRs induce Ca(2+) release from intracellular stores, whereas P2XRs are Ca(2+)-permeable ion channels. Depletion of [Ca(2+)](i) stores with thapsigargin (TG) prevented the ATP-induced increase in [Ca(2+)](i) in zero, but not in 2 mM [Ca(2+)](o), indicating that both Ca(2+) influx and release of intracellular Ca(2+) contribute to the ATP response. Ca(2+) influx was partially blocked by cadmium, indicating a contribution of voltage-gated Ca(2+) channels. PPADS (pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid), and iso-PPADS, P2XR antagonists, attenuated, but did not abolish, the ATP-induced increase in [Ca(2+)](i). Combined treatment with PPADS or iso-PPADS and TG prevented the response. A cocktail of P2YR agonists consisting of UTP, UDP, and 2-methylthio-ADP increased [Ca(2+)](i) (with or without tetrodotoxin) that was markedly attenuated by TG. 2-Methylthio-ADP alone induced consistent and larger increases in [Ca(2+)](i) than UTP or UDP. MRS2179, a specific P2Y(1)R antagonist, eliminated the response to ATP in zero [Ca(2+)](o). Thus, both P2XR and P2YR participate in the ATP-induced increase in [Ca(2+)](i), and the P2Y(1)R subtype is more prominent than P2Y(2)R, P2Y(4)R, or P2Y(6)R in SON.

Authors+Show Affiliations

Department of Physiology and Biophysics, University of Colorado at Denver and Health Sciences Center, P.O. Box 6511, Mail Stop 8307, Aurora, CO 80045, USA. zhilin.song@uchsc.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

16973929

Citation

Song, Zhilin, et al. "ATP Increases Intracellular Calcium in Supraoptic Neurons By Activation of Both P2X and P2Y Purinergic Receptors." American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, vol. 292, no. 1, 2007, pp. R423-31.
Song Z, Vijayaraghavan S, Sladek CD. ATP increases intracellular calcium in supraoptic neurons by activation of both P2X and P2Y purinergic receptors. Am J Physiol Regul Integr Comp Physiol. 2007;292(1):R423-31.
Song, Z., Vijayaraghavan, S., & Sladek, C. D. (2007). ATP increases intracellular calcium in supraoptic neurons by activation of both P2X and P2Y purinergic receptors. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 292(1), R423-31.
Song Z, Vijayaraghavan S, Sladek CD. ATP Increases Intracellular Calcium in Supraoptic Neurons By Activation of Both P2X and P2Y Purinergic Receptors. Am J Physiol Regul Integr Comp Physiol. 2007;292(1):R423-31. PubMed PMID: 16973929.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - ATP increases intracellular calcium in supraoptic neurons by activation of both P2X and P2Y purinergic receptors. AU - Song,Zhilin, AU - Vijayaraghavan,Sukumar, AU - Sladek,Celia D, Y1 - 2006/09/14/ PY - 2006/9/16/pubmed PY - 2007/2/9/medline PY - 2006/9/16/entrez SP - R423 EP - 31 JF - American journal of physiology. Regulatory, integrative and comparative physiology JO - Am. J. Physiol. Regul. Integr. Comp. Physiol. VL - 292 IS - 1 N2 - ATP increases intracellular calcium concentration ([Ca(2+)](i)) in supraoptic nucleus (SON) neurons in hypothalamo-neurohypophyseal system explants loaded with the Ca(2+)-sensitive dye, fura 2-AM. Involvement of P2X purinergic receptors (P2XR) in this response was anticipated, because ATP stimulation of vasopressin release from hypothalamo-neurohypophyseal system explants required activation of P2XRs, and activation of P2XRs induced an increase in [Ca(2+)](i) in dissociated SON neurons. However, the ATP-induced increase in [Ca(2+)](i) persisted after removal of Ca(2+) from the perifusate ([Ca(2+)](o)). This suggested involvement of P2Y purinergic receptors (P2YR), because P2YRs induce Ca(2+) release from intracellular stores, whereas P2XRs are Ca(2+)-permeable ion channels. Depletion of [Ca(2+)](i) stores with thapsigargin (TG) prevented the ATP-induced increase in [Ca(2+)](i) in zero, but not in 2 mM [Ca(2+)](o), indicating that both Ca(2+) influx and release of intracellular Ca(2+) contribute to the ATP response. Ca(2+) influx was partially blocked by cadmium, indicating a contribution of voltage-gated Ca(2+) channels. PPADS (pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid), and iso-PPADS, P2XR antagonists, attenuated, but did not abolish, the ATP-induced increase in [Ca(2+)](i). Combined treatment with PPADS or iso-PPADS and TG prevented the response. A cocktail of P2YR agonists consisting of UTP, UDP, and 2-methylthio-ADP increased [Ca(2+)](i) (with or without tetrodotoxin) that was markedly attenuated by TG. 2-Methylthio-ADP alone induced consistent and larger increases in [Ca(2+)](i) than UTP or UDP. MRS2179, a specific P2Y(1)R antagonist, eliminated the response to ATP in zero [Ca(2+)](o). Thus, both P2XR and P2YR participate in the ATP-induced increase in [Ca(2+)](i), and the P2Y(1)R subtype is more prominent than P2Y(2)R, P2Y(4)R, or P2Y(6)R in SON. SN - 0363-6119 UR - https://www.unboundmedicine.com/medline/citation/16973929/ATP_increases_intracellular_calcium_in_supraoptic_neurons_by_activation_of_both_P2X_and_P2Y_purinergic_receptors_ L2 - http://www.physiology.org/doi/full/10.1152/ajpregu.00495.2006?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -