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BIBTEX RIS

Involvement of chloride channel coupled GABAC receptors in the peripheral antinociceptive effect induced by GABAC receptor agonist cis-4-aminocrotonic acid

2007; Elsevier BV; Volume: 80; Issue: 14 Linguagem: Inglês

10.1016/j.lfs.2006.12.015

1879-0631

Gláucia Maria Lopes Reis, Igor Dimitri Gama Duarte,

Botulinum Toxin and Related Neurological Disorders

We investigated the effect of chloride and potassium channel blockers on the antinociception induced by GABAC receptor agonist CACA (cis-4-aminocrotonic acid) using the paw pressure test, in which pain sensitivity was increased by an intraplantar injection (2 μg) of prostaglandin E2 (PGE2). CACA administered locally into the right hindpaw (25, 50 and 100 μg/paw) elicited a dose-dependent antinociceptive effect which was demonstrated to be local, since only higher doses produced an effect when injected in the contralateral paw. The GABAC receptor antagonist (1,2,5,6 tetrahydropyridin-4-yl) methylphosphinic acid (TPMPA; 5, 10 and 20 μg/paw) antagonized, in a dose-dependent manner, the peripheral antinociception induced by CACA (100 μg), suggesting a specific effect. This effect was reversed by the chloride channel coupled receptor blocker picrotoxin (0.8 μg/paw). Glibenclamide (160 μg) and tolbutamide (320 μg), blockers of ATP-sensitive potassium channels, charybdotoxin (2 μg), a large-conductance potassium channel blocker, dequalinium (50 μg), a small-conductance potassium channel blocker, and cesium (500 μg), a non-specific potassium channel blocker did not modify the peripheral antinociception induced by CACA. This study provides evidence that activation of GABAC receptors in the periphery induces antinociception, that this effect results from the activation of chloride channel coupled GABAC receptors and that potassium channels appear not to be involved.