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Decreased inflammatory pain due to reduced carrageenan-induced inflammation in mice lacking adenosine A3 receptors.

Abstract
Mice with a targeted disruption of adenosine A(3) receptor (A(3)AR) gene were assessed for their nociceptive threshold and for their localized inflammatory response following carrageenan injected into the hindpaw. Under basal conditions no difference was seen between A(3)AR knock-out (A(3)AR(-/-)) and wild-type (A(3)AR(+/+)) mice in nociceptive response to mechanical or heat stimuli. The antinociceptive response to the intrathecal adenosine analogue R-phenylisopropyl adenosine (R-PIA) was also unchanged in the A(3)AR(-/-) mice. In contrast, heat hyperalgesia, plasma extravasation and edema following carrageenan-induced inflammation in the hind paw were significantly reduced in A(3)AR(-/-) mice compared to the A(3)AR(+/+) controls. Thus, mice lacking A(3)AR had deficits in generating the localized inflammatory response to carrageenan, supporting a pro-inflammatory role of A(3)AR in peripheral tissues. However, no evidence for a role of A(3)AR in nociception and the antinociceptive effect of R-PIA was found.
AuthorsW-P Wu, J-X Hao, L Halldner-Henriksson, X-J Xu, M A Jacobson, Z Wiesenfeld-Hallin, B B Fredholm
JournalNeuroscience (Neuroscience) Vol. 114 Issue 3 Pg. 523-7 ( 2002) ISSN: 0306-4522 [Print] United States
PMID12220556 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright 2002 IBRO
Chemical References
  • Receptor, Adenosine A3
  • Receptors, Purinergic P1
  • Carrageenan
Topics
  • Animals
  • Carrageenan (adverse effects)
  • Inflammation (chemically induced, genetics, metabolism)
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Pain (chemically induced, genetics, metabolism, pathology)
  • Pain Measurement (methods)
  • Pain Threshold (physiology)
  • Receptor, Adenosine A3
  • Receptors, Purinergic P1 (deficiency, genetics)

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