ABSTRACT
It was shown that cannabinoids anandamide, HU210 and WIN 55,212-2 inhibit both spontaneous episodes of pain and mechanical allodynia in rats with central pain syndrome caused by disturbance of inhibitory processes in the dorsal horns of lumbar spinal cord. The analgesic effect is most pronounced in the intrathecal route of administration. The intensity of analgesic actions of cannabinoids on the central pain syndrome in rats, depending on the drug is as follows: HU210 > WIN 55,212-2 > anandamide.
Subject(s)
Analgesics, Non-Narcotic/pharmacology , Back Pain/drug therapy , Back Pain/physiopathology , Cannabinoids/pharmacology , Spinal Cord/physiopathology , Animals , Back Pain/pathology , Dose-Response Relationship, Drug , Hyperalgesia/drug therapy , Hyperalgesia/pathology , Hyperalgesia/physiopathology , Lumbosacral Region/pathology , Lumbosacral Region/physiopathology , Rats , Rats, Wistar , Spinal Cord/pathologySubject(s)
Cannabinoid Receptor Agonists , Cannabinoid Receptor Antagonists , Cannabinoid Receptor Modulators/physiology , Analgesics/adverse effects , Analgesics/pharmacology , Analgesics/therapeutic use , Animals , Cannabinoids/adverse effects , Cannabinoids/pharmacology , Cannabinoids/therapeutic use , Drug Tolerance , Humans , Ligands , Pain/drug therapy , Pain/metabolism , Receptors, Cannabinoid/physiologyABSTRACT
Essential distinctions in the neurophysiologic and neurochemical mechanisms related with the shaping of pain syndromes presuppose the administration of different-action analgetics in coping with such syndromes. Data, obtained recently in studying the fundamental mechanisms of nociception and analgesia, denote a variety of new "targets" for potential analgetics, i.e. cannabinoid receptors, NMDA-receptors of subtype NR2B, kainate and metabotropic receptors, central n-cholinergic receptors, vanilloid receptors and purinoceptors, tetrodotoxin-insensitive sodium channel SNS/PN3, calcium channels of N-type and gabapenti-binding protein.
