Facial nerve lesions lead to increased immunostaining of the astrocytic gap junction protein (connexin 43) in the corresponding facial nucleus of rats.

After peripheral transection of the facial nerve, immunostaining of astrocytic gap junction protein changed in the corresponding brainstem nucleus of the rat. Enhanced connexin-43 immunoreactivity was restricted to the ipsilateral facial nucleus and to astrocytes surrounding lesioned motoneurons. This reaction is focally distinct, and marks only a part of the astrocytic network indicating a local plasticity of intercellular coupling. These results suggest that astrocytes work as sensors of signals which either depend on the integrity of neighboring neurons or inform about neuronal disorders.