Abstract
In this work, we studied transgenic glial fibrillary acidic protein-IkappaBalpha-dn mice that selectively inactivate the classical nuclear factor kappaB pathway by overexpressing the inhibitory protein of kappaBalpha in astrocytes, under the control of glial fibrillary acidic protein promoter. We sought to determine if glial nuclear factor kappaB inhibition decreases formalin pain. Formalin testing was carried out on 25-35 g littermate adult male wild-type and transgenic C57Bl/6 mice. Formalin increased spinal cord c-Fos expression and glial fibrillary acidic protein immunostaining in both wild-type and transgenic mice. Transgenic glial fibrillary acidic protein-inhibitory protein of kappaBalpha-dn mice had lower duration of formalin-induced paw-licking behavior. These data support a role of glial nuclear factor kappaB inhibition in reducing pain after peripheral nerve inflammation.
