HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Reber, B F Articles by Reuter, H Search for Related Content PubMed PubMed Citation Articles by Reber, B F Articles by Reuter, H

Department of Pharmacology, University of Bern, Switzerland.

1. A clone of the rat phaeochromocytoma cell line (PC12) was treated with nerve growth factor (NGF) for 4-6 days and used to study caffeine- and bradykinin-induced Ca2+ release from intracellular Ca2+ stores. The caffeine-sensitive store can be depleted by Ca(2+)-induced Ca2+ release (CICR), while the bradykinin-induced release is mediated by inositol 1,4,5-trisphosphate (IP3). The effect of Ca2+ release from these Ca2+ stores on cytosolic free Ca2+ ([Ca2+]i) was measured by means of fura-2 single cell microfluorimetry. 2. Caffeine application caused no or only a small Ca2+ release in untreated cells in normal culture medium. The caffeine-sensitive pool could be filled by Ca2+ entry into cells through either voltage-activated Ca2+ channels or ligand-gated cation channels. 3. Bradykinin application produced substantial Ca2+ release in untreated cells in normal culture medium. The response was enhanced after K(+)-depolarization of the cells. The bradykinin-induced release of Ca2+ also caused depletion of the caffeine-sensitive pool by CICR. However, Ca2+ released from the IP3-sensitive store was not sequestered into the caffeine-sensitive Ca2+ store. 4. The caffeine-induced rise in [Ca2+]i was blocked by ryanodine in a use-dependent manner. In addition, a substantial use-dependent ryanodine block resulted from the bradykinin-induced rise of [Ca2+]i and subsequent CICR. By contrast, the K(+)-induced rise of [Ca2+]i caused only a marginal use-dependent ryanodine inhibition of Ca2+ release. 5. Our results suggest an enhancement of the IP3-induced [Ca2+]i rise in the cytoplasm by CICR from the caffeine-sensitive pool. 6. A mathematical model adequately simulates our experimental data.

This article has been cited by other articles:

				M. Cataldi, V. Lariccia, A. Secondo, G. di Renzo, and L. Annunziato The Antiepileptic Drug Levetiracetam Decreases the Inositol 1,4,5-Trisphosphate-Dependent [Ca2+]i Increase Induced by ATP and Bradykinin in PC12 Cells J. Pharmacol. Exp. Ther., May 1, 2005; 313(2): 720 - 730. [Abstract] [Full Text] [PDF]

				A. Verkhratsky Physiology and Pathophysiology of the Calcium Store in the Endoplasmic Reticulum of Neurons Physiol Rev, January 1, 2005; 85(1): 201 - 279. [Abstract] [Full Text] [PDF]

				D. J. Fickbohm and A. L. Willard Upregulation of Calcium Homeostatic Mechanisms in Chronically Depolarized Rat Myenteric Neurons J Neurophysiol, June 1, 1999; 81(6): 2683 - 2695. [Abstract] [Full Text] [PDF]

				M. Solem, T. McMahon, and R. O. Messing Protein Kinase A Regulates Inhibition of N- and P/Q-type Calcium Channels by Ethanol in PC12 Cells J. Pharmacol. Exp. Ther., September 1, 1997; 282(3): 1487 - 1495. [Abstract] [Full Text]

				P. Pizzo, C. Fasolato, and T. Pozzan Dynamic Properties of an Inositol 1,4,5-Trisphosphate- and Thapsigargin-insensitive Calcium Pool in Mammalian Cell Lines J. Cell Biol., January 27, 1997; 136(2): 355 - 366. [Abstract] [Full Text] [PDF]