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Spinal pharmacology of tactile allodynia in diabetic rats
Author(s) -
Calcutt Nigel A.,
Chaplan Sandra R.
Publication year - 1997
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0701538
Subject(s) - allodynia , medicine , pharmacology , nmda receptor , agonist , receptor antagonist , nociception , hyperalgesia , anesthesia , antagonist , endocrinology , receptor
1 Rats develop tactile allodynia to stimulation of the plantar surface of the hindpaw with von Frey filaments within days of the onset of streptozotocin‐induced diabetes. This is prevented by insulin and alleviated by systemic lignocaine, but the aetiology is unknown. 2 Using indwelling lumbar intrathecal catheters to deliver pharmacological agents, we have investigated whether tactile allodynia in streptozotocin‐diabetic rats is dependent on mechanisms associated with spinal sensitization, by assessing the efficacy of agents that inhibit specific components of spinal nociceptive processing. 3 Dose‐dependent inhibition of tactile allodynia in diabetic rats was noted with the N‐type calcium channel antagonist SNX 239, the α 2 ‐adrenoceptor agonist dexmedetomidine, the μ‐opioid receptor agonist morphine, the N‐methyl‐ D ‐aspartate (NMDA) receptor antagonist AP5 and the non‐NMDA receptor antagonist NBQX. 4 No effect on tactile allodynia was noted after intrathecal administration of the nitric oxide synthase inhibitor N G ‐nitro‐ L ‐arginine methyl ester ( L ‐NAME), the cyclo‐oxygenase inhibitor ketorolac, the L‐type calcium channel inhibitor diltiazem or any vehicle. 5 These data suggest that the tactile allodynia of diabetic rats involves spinal glutamatergic pathways but is not associated with spinal release of nitric oxide or prostaglandins.