L-NAME, an inhibitor of nitric oxide synthase, blocks the established allodynia induced by intrathecal administration of prostaglandin E2.

Abstract

We recently reported that intrathecal (i.t.) administration of prostaglandin E2 (PGE2) to conscious mice induced allodynia, a state of discomfort and pain evoked by innocuous tactile stimuli. In the present study, we examined the effect of the PGE receptor EP1 subtype antagonist ONO-NT-012, the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801, and the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) on the allodynia. The PGE2-induced allodynia was blocked by simultaneous i.t. injection of ONO-NT-012, MK-801, or L-NAME. However, 5 min after i.t. injection of PGE2, the allodynia was significantly blocked by i.t. L-NAME, but not by i.t. ONO-NT-012 or MK-801. These results demonstrate that the PGE2-induced allodynia, once developed, does not require the continued agonist occupancy of EP1 and NMDA glutamate receptor sites.

• Authors: T Minami, M Onaka, E Okuda-Ashitaka, H Mori, S Ito, O Hayaishi
• Journal: Neuroscience letters (Neurosci Lett) Vol. 201 Issue 3 Pg. 239-42 (Dec 15 1995) ISSN: 0304-3940 [Print] Ireland
• PMID: 8786849 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Enzyme Inhibitors
• Arginine
• Dinoprostone
• NG-Nitroarginine Methyl Ester

Topics

• Animals
• Arginine (analogs & derivatives, pharmacology)
• Dinoprostone (pharmacology)
• Dose-Response Relationship, Drug
• Enzyme Inhibitors (pharmacology)
• Injections, Spinal
• Male
• Mice
• Mice, Inbred Strains
• NG-Nitroarginine Methyl Ester
• Pain (metabolism)
• Spinal Cord (drug effects)