Open AccessSpinal Opioid Receptor Like1 Receptor Agonist, but Not N-Methyl-d-Aspartic Acid Antagonist, Reverses the Secondary Mechanical Allodynia Induced by Intradermal Injection of Capsaicin in Rats
Author(s) -
Natsuko Nozaki-Taguchi,
Tatsuo Yamamoto
Publication year - 2005
Publication title -
anesthesia and analgesia/anesthesia and analgesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.404
H-Index - 201
eISSN - 1526-7598
pISSN - 0003-2999
DOI - 10.1213/01.ane.0000147509.01309.eb
Subject(s) - nociceptin receptor , allodynia , medicine , capsaicin , receptor antagonist , pharmacology , agonist , opioid , anesthesia , hyperalgesia , receptor , antagonist , nociception , opioid peptide
Secondary mechanical allodynia induced by intradermal injection of capsaicin has been widely used to search for the underlying mechanisms of tissue injury induced mechanical allodynia. However, the capsaicin concentration dependency of the development of secondary mechanical allodynia and the underlying mechanisms of development and maintenance of capsaicin-induced mechanical allodynia are not fully understood. In the present study, we clarify the capsaicin concentration dependency for development and maintenance of secondary mechanical allodynia and the role of spinal opioid receptor like1 (ORL1) receptor and N-methyl-D-aspartate receptor in the development and maintenance of secondary mechanical allodynia induced by an intradermal capsaicin injection. Capsaicin 50 microL of 0.03% induced the most intense secondary mechanical allodynia. Intrathecal injection of nociceptin, an ORL1 receptor agonist, attenuated the maintenance of secondary mechanical allodynia but had no effect on the development of secondary mechanical allodynia. An intrathecal injection of MK801, an N-methyl-D-aspartate receptor antagonist, had no effect on the development and maintenance of secondary mechanical allodynia. These findings suggest that spinal ORL1 receptor should be the target of study for the treatment of secondary mechanical allodynia induced by tissue injury.