Cannabinoid subtype-2 receptors modulate the antihyperalgesic effect of WIN 55,212-2 in rats with neuropathic spinal cord injury pain

Peripheral antinociceptive effect of anandamide and drugs that affect the endocannabinoid system on the formalin test in normal and streptozotocin-diabetic rats

“…Accordingly, the endocannabinoid system has been named as one of the most promising target of chronic pain pharmacotherapy (Di Marzo and Petrocellis, 2006) including neuropathic pain states (Ahmed et al, 2010;Guindon and Beaulieu, 2006;Hasanein and Soltani, 2009). The endocannabinoid system comprises endogenous cannabinoid receptor ligands such as N-arachidonoyl ethanolamide (anandamide; Devane et al, 1992) and 2-arachidonoylglycerol (2-AG; Sugiura et al, 1995), both CB1 and CB2 cannabinoid receptors (Matsuda et al, 1990), enzymes that catalyze the endocannabinoids synthesis, N-acylphosphatidyletanolamide-specific phospholipase D (Di Marzo et al, 1994) and diacylglycerol lipase (Piomelli, 2003), enzymes responsible for degradation, fatty acid amide hydrolase and monoacylglycerol lipase (Piomelli, 2003), and endocannabinoids reuptake transporters (for review see Guindon and Hohmann, 2009).…”

The Interaction Between Intrathecal Administration of Low Doses of Palmitoylethanolamide and AM251 in Formalin-Induced Pain Related Behavior and Spinal Cord IL1-β Expression in Rats

“…Other suggested mechanism is the so-called ''entourage effect'' due to the PEA-induced inhibition of the enzyme catalyzing the endocannabinoid anandamide (AEA) degradation which may lead to an enhancement of its tissue levels thus increasing its analgesic action [25]. In a study by Ahmed et al [26], systemically administration of WIN55212-2 significantly ameliorated thermal hyperalgesia after spinal cord injury. The effect of WIN55212-2 was blocked by AM630, but not AM251, pretreatment; suggesting a role of the CB2 receptor, but not CB1 receptor, in spinal injuryrelated hyperalgesia.…”

Immediate administration of COX inhibitors in spinal cord contusion injury and a current review of COX Therapy

“…For celecoxib and indomethacin administration experiments, each animal received a contusion SCI (cSCI) at the T9 level using the New York University (NYU) impactor by dropping a 10 gram rod from 12.5 mm an established contusion SCI and NP rat model [9,[12][13][14][15]17,[34][35][36].…”

“…This test is being routinely employed in our SCI/NP rat model in our lab [12][13][14][15]17,37]. An animal placed inside a plastic box on a raised glass cord injury neuropathic pain (SCINP) is not very clear.…”

“…Employing a rat model of contusion SCI, research in our lab has been focused on the use of cyclooxygenase 2 (COX-2) inhibitors during the acute phase of SCI [7]. Chronic phase studies of SCI-induced injuries, reviewed from our lab [8] focused on numerous pathways including the use of peroxisome proliferator-activated receptor (PPAR-gamma) agonists [9] ; COX-2 inhibitors [10,11]; vanilloid-1/ bradykinin-1 receptor antagonists [12]; phosphodiesterase-4 (PDE4) inhibitor, rolipram [13]; cannabinoid (CB1/CB2) receptors [14]; ion channel activity including NKCC1/KCC2 in the development of chronic NP [15][16][17][18].…”