P2 Purinoceptors and Pyrimidinoceptors of Catecholamine-Producing Cells and Immunocytes

  1. Derek J. Chadwick Organizer and
  2. Jamie A. Goode
  1. P. Illes,
  2. K. Nieber,
  3. R. Fröhlich and
  4. W. Nörenberg

Published Online: 28 SEP 2007

DOI: 10.1002/9780470514900.ch6

Ciba Foundation Symposium 198 - P2 Purinoceptors: Localization, Function and Transduction Mechanisms

Ciba Foundation Symposium 198 - P2 Purinoceptors: Localization, Function and Transduction Mechanisms

How to Cite

Illes, P., Nieber, K., Fröhlich, R. and Nörenberg, W. (2007) P2 Purinoceptors and Pyrimidinoceptors of Catecholamine-Producing Cells and Immunocytes, in Ciba Foundation Symposium 198 - P2 Purinoceptors: Localization, Function and Transduction Mechanisms (eds D. J. Chadwick and J. A. Goode), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470514900.ch6

Author Information

  1. Institut für Pharmakologie und Toxikologie der Universität Freiburg, Hermann-Herder Strasse 5, D-79104 Freiburg, Germany

  1. Institut für Pharmakologie und Toxikologie der Universität Leipzig, Härtelstrasse 16-18, D-04107 Leipzig, Germany

  2. Institut für Pharmazie der Universität, Abteilung Pharmakologie für Naturwissenschaftler, Brüderstrasse 34, D-04103 Leipzig, Germany

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471961253

Online ISBN: 9780470514900

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Keywords:

  • P2 purinoceptors;
  • pyrimidinoceptors;
  • catecholamirse-producing cells;
  • immunocytes;
  • P2Y purinoceptors

Summary

ATP is a neuronal (co)transmitter. In addition, both ATP and UTP may exit damaged cells and thereby function as extracellular signal molecules. The targets of signalling may be the P2 (for ATP and UTP) and P1 (for the degradation product adenosine) receptors of, for instance, neurons and immunocytes. UTP may also act at separate pyrimidinoceptors. Catecholamine-producing cells (adrenal chromaffin cells and peripheral and central noradrenergic neurons) possess P2X and P2Y purinoceptors. ATP appears to be a fast excitatory neuro-neuronal transmitter of the noradrenergic coeliac and locus coeruleus neurons. This effect is mediated by P2X purinoceptors. P2Y purinoceptor-mediated slow excitatory synaptic potentials have not yet been demonstrated either in the peripheral or central nervous system. On the other hand, after neuronal injury microglial cells (brain immunocytes) are engaged in a process called ‘synaptic stripping’, i.e. the displacement of synaptic boutons from the neuronal surface. During this process microglial cells are in direct contact with the (co)transmitter ATP. Activation of P2X, P2Z and P2Y purinoceptors results in an elevated intracellular Ca2+ concentration in microglia and macrophages. Various functions of these cells are regulated by intracellular Ca2+ (e.g. cytokine production, phagocytosis) and may therefore be modulated by nucleotides. Since neuronal damage leads to the transformation of microglial cells to macrophages and, at the same time, to the efflux of nucleotides from the damaged cells, the requirements for a modulatory interaction are fulfilled.