title: Modulation of neuropathic-pain-related behaviour by the spinal endocannabinoid/endovanilloid system.
abstract: Neuropathic pain refers to chronic pain that results from injury to the nervous system. The mechanisms involved in neuropathic pain are complex and involve both peripheral and central phenomena. Although numerous pharmacological agents are available for the treatment of neuropathic pain, definitive drug therapy has remained elusive. Recent drug discovery efforts have identified an original neurobiological approach to the pathophysiology of neuropathic pain. The development of innovative pharmacological strategies has led to the identification of new promising pharmacological targets, including glutamate antagonists, microglia inhibitors and, interestingly, endogenous ligands of cannabinoids and the transient receptor potential vanilloid type 1 (TRPV1). Endocannabinoids (ECs), endovanilloids and the enzymes that regulate their metabolism represent promising pharmacological targets for the development of a successful pain treatment. This review is an update of the relationship between cannabinoid receptors (CB1) and TRPV1 channels and their possible implications for neuropathic pain. The data are focused on endogenous spinal mechanisms of pain control by anandamide, and the current and emerging pharmacotherapeutic approaches that benefit from the pharmacological modulation of spinal EC and/or endovanilloid systems under chronic pain conditions will be discussed.
authors.affiliation: Department of Pain Pharmacology, Institute of Pharmacology, Polish Academy of Sciences, ul. Smetna 12, 31-343 Krakow, Poland. starow@if-pan.krakow.pl
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Starowicz
authors.forename: Barbara
authors.initials: B
authors.lastname: Przewlocka
mesh_terms: D000577:Amides; D000581:Amidohydrolases / Q000037:antagonists & inhibitors* / Q000378:metabolism; D000818:Animals; D016718:Arachidonic Acid / Q000378:metabolism; D001095:Arachidonic Acids / Q000378:metabolism* / Q000494:pharmacology; D001519:Behavior / Q000187:drug effects*; D001549:Benzamides / Q000494:pharmacology; D002219:Carbamates / Q000494:pharmacology; D063388:Endocannabinoids / Q000378:metabolism* / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004983:Ethanolamines / Q000378:metabolism; D005989:Glycerides / Q000378:metabolism; D006801:Humans; D017628:Microglia / Q000187:drug effects / Q000378:metabolism; D009437:Neuralgia / Q000188:drug therapy / Q000503:physiopathology* / Q000523:psychology*; D010169:Palmitic Acids / Q000378:metabolism; D059348:Peripheral Nerve Injuries / Q000188:drug therapy / Q000503:physiopathology; D053284:Polyunsaturated Alkamides / Q000378:metabolism* / Q000494:pharmacology; D043884:Receptor, Cannabinoid, CB1 / Q000378:metabolism*; D013119:Spinal Cord Injuries / Q000188:drug therapy / Q000503:physiopathology; D050916:TRPV Cation Channels / Q000378:metabolism; D000099252:Fatty Acid Amide Hydrolases
chemical_list: D000577:Amides; D000581:Amidohydrolases; D016718:Arachidonic Acid; D001095:Arachidonic Acids; D001549:Benzamides; D002219:Carbamates; D063388:Endocannabinoids; D004791:Enzyme Inhibitors; D004983:Ethanolamines; D005989:Glycerides; D010169:Palmitic Acids; D053284:Polyunsaturated Alkamides; D043884:Receptor, Cannabinoid, CB1; D050916:TRPV Cation Channels; D000099252:Fatty Acid Amide Hydrolases; C494482:TRPV1 protein, human; C500528:cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester; C005958:palmidrol; C094503:glyceryl 2-arachidonate; C078814:anandamide