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

  title={Actions of N-arachidonyl-glycine in a rat neuropathic pain model},
  author={Le Quang Vuong and Vanessa A. Mitchell and Christopher W. Vaughan},
Actions of N-arachidonyl-glycine in a rat inflammatory pain model
The findings suggest that NA-glycine may provide a novel non-cannabinoid receptor mediated approach to alleviate inflammatory pain.
The Endogenous Cannabinoid System: A Budding Source of Targets for Treating Inflammatory and Neuropathic Pain
Preclinical and clinical evidence of various endocannabinoid system targets as potential therapeutic strategies for inflammatory and neuropathic pain conditions are examined.
T-Type Calcium Channel Inhibition Underlies the Analgesic Effects of the Endogenous Lipoamino Acids
It is demonstrated here that lipoamino acids NAGly and NAGABA-OH produced a strong thermal analgesia and that these effects were abolished in Cav3.2 knock-out mice, suggesting that these ligands can modulate multiple cell functions via this newly evidenced regulation.
Extracellular Loops 2 and 4 of GLYT2 Are Required for N-Arachidonylglycine Inhibition of Glycine Transport*
Observations suggest that the structure of the head group of these compounds is important in determining how they interact with extracellular loops 2 and 4 of GLYT2.
Cannabinoids as pharmacotherapies for neuropathic pain: From the bench to the bedside
N-Arachidonyl Glycine Does Not Activate G Protein–Coupled Receptor 18 Signaling via Canonical Pathways
GPR18 coupling in a native neuronal system with endogenous signaling pathways and effectors is investigated, suggesting NAGly is not an agonist for GPR18 or that G PR18 signaling involves noncanonical pathways not examined in these studies.
Development of an N-Acyl Amino Acid That Selectively Inhibits the Glycine Transporter 2 To Produce Analgesia in a Rat Model of Chronic Pain.
It is demonstrated that 33 provides greater analgesia at lower doses, and does not possess the severe side effects of the very slowly reversible GlyT2 inhibitor, ORG25543 (2).


Actions of the FAAH inhibitor URB597 in neuropathic and inflammatory chronic pain models
It is suggested that the FAAH inhibitor URB597 produces cannabinoid CB1 and CB2 receptor‐mediated analgesia in inflammatory pain states, without causing the undesirable side effects associated with cannabinoid receptor activation.
The synthetic cannabinoid WIN55,212‐2 attenuates hyperalgesia and allodynia in a rat model of neuropathic pain
The data indicate that cannabinoids may have therapeutic potential in neuropathic pain, and that this effect is mediated through the CB1 receptor.
CB2 receptor‐mediated antihyperalgesia: possible direct involvement of neural mechanisms
It is suggested that CB2 agonists may elicit their analgesic effect by acting not only at non‐neuronal peripheral sites but also at neural level, making CB2 an attractive target for chronic pain treatment.
Inhibitory effects of CB1 and CB2 receptor agonists on responses of DRG neurons and dorsal horn neurons in neuropathic rats
At the level of the spinal cord, CB2 receptors have inhibitory effects in neuropathic, but not sham‐operated rats suggesting that spinal CB2 may be an important analgesic target.
Induction of CB2 receptor expression in the rat spinal cord of neuropathic but not inflammatory chronic pain models
It is reported here that chronic pain models associated with peripheral nerve injury, but not peripheral inflammation, induce CB2 receptor expression in a highly restricted and specific manner within the lumbar spinal cord.
Selective oxygenation of N-arachidonylglycine by cyclooxygenase-2.