Email updates

Keep up to date with the latest news and content from Molecular Pain and BioMed Central.

Open Access Open Badges Short report

Actions of N-arachidonyl-glycine in a rat inflammatory pain model

Rebecca Succar, Vanessa A Mitchell and Christopher W Vaughan*

Author Affiliations

Pain Management Research Institute, Northern Clinical School, The University of Sydney at Royal North Shore Hospital, St Leonards, 2065, NSW, Australia

For all author emails, please log on.

Molecular Pain 2007, 3:24  doi:10.1186/1744-8069-3-24

Published: 30 August 2007



While cannabinoid receptor agonists have analgesic activity in inflammatory pain states they produce a range of side effects. Recently, it has been demonstrated that the arachidonic acid-amino acid conjugate, N-arachidonyl-glycine (NA-glycine) is effective in acute pain models.


In the present study we examined the effect of NA-glycine in a rat model of inflammatory pain. Intrathecal administration of NA-glycine (70 – 700 nmol) and the pan-cannabinoid receptor agonist HU-210 (10 nmol) reduced the mechanical allodynia and thermal hyperalgesia induced by intraplantar injection of Freund's complete adjuvant (FCA). The actions of HU-210, but not NA-glycine were reduced by the cannabinoid CB1 receptor antagonist AM251. The cannabinoid CB2 receptor antagonist SR144528 also had no effect on the actions of NA-glycine. In contrast, N-arachidonyl-GABA (NA-GABA, 700 nmol) and N-arachidonyl-alanine (NA-alanine, 700 nmol) had no effect on allodynia and hyperalgesia. HU-210, but not NA-glycine produced a reduction in rotarod latency.


These findings suggest that NA-glycine may provide a novel non-cannabinoid receptor mediated approach to alleviate inflammatory pain.