Skip to main content
British Journal of Pharmacology logoLink to British Journal of Pharmacology
. 1997 Dec;122(7):1478–1482. doi: 10.1038/sj.bjp.0701538

Spinal pharmacology of tactile allodynia in diabetic rats

Nigel A Calcutt *,*, Sandra R Chaplan *
PMCID: PMC1565094  PMID: 9421298

Abstract

  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 α2-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 NG-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.

Keywords: Diabetes, diabetic neuropathy, pain, allodynia, glutamate receptor, spinal cord

Full Text

The Full Text of this article is available as a PDF (296.9 KB).


Articles from British Journal of Pharmacology are provided here courtesy of The British Pharmacological Society

RESOURCES