+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: found

      Activation of Muscarinic and Serotonergic Receptors Results in Phosphoinositide Hydrolysis but Not in Mobilization of Calcium in Sympathetic Neurons

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          The effects of various neurotransmitters on phosphoinositide hydrolysis, mobilization of Ca<sup>2+</sup> and release of [<sup>3</sup>H]-norepinephrine ([<sup>3</sup>H]-NE) were studied in cultures of sympathetic neurons of chick embryos. [<sup>3</sup>H]-inositol-1,4,5-triphosphate ([<sup>3</sup>H]-IP<sub>3</sub>) was increased in sympathetic neurons by acetylcholine (ACh), muscarine and serotonin (5-HT). Dopamine and norepinephrine did not stimulate phosphoinositide hydrolysis. Intracellular concentration of free Ca<sup>2+</sup> ([Ca<sup>2+</sup>]<sub>i</sub>) was measured in Indo-1-loaded sympathetic neurons at rest and after addition of test agents. Measurements were made in the cell body and growth cone regions since Ca<sup>2+</sup> mobilization is known to be different in different regions of the sympathetic neurons. ACh (nicotinic component was blocked by hexamethonium) and 5-HT failed to increase the [Ca<sup>2+</sup>]<sub>i</sub>, in the cell body as well as in the growth cone. The spontaneous release of [<sup>3</sup>H]-NE was not affected by ACh and 5-HT. Caffeine increased the [Ca<sup>2+</sup>]<sub>i</sub> only in the cell body but not in the growth cone and had no effect on the release of [<sup>3</sup>H]-NE. These results suggest that an IP3-insensitive but caffeine-sensitive pool of Ca<sup>2+</sup> is present only in the somatic region of sympathetic neurons and is not coupled to the transmitter release.

          Related collections

          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          23 September 2008
          : 28
          : 1-3
          : 6-10
          Department of Pharmacology, Wayne State University, School of Medicine, Detroit, Mich., USA
          158837 Blood Vessels 1991;28:6–10
          © 1991 S. Karger AG, Basel

          Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

          Page count
          Pages: 5
          Neuronal Control of Vascular Function


          Comment on this article