%0 Journal Article
%T Differential cellular FGF-2 upregulation in the rat facial nucleus following axotomy, functional electrical stimulation and corticosterone: a possible therapeutic target to Bell's palsy
%A Karen F Coracini
%A Caio J Fernandes
%A Almir F Barbarini
%A C¨¦sar M Silva
%A Rodrigo T Scabello
%A Gabriela P Oliveira
%A Gerson Chadi
%J Journal of Brachial Plexus and Peripheral Nerve Injury
%D 2010
%I Thieme Medical Publishers
%R 10.1186/1749-7221-5-16
%X Adult rats received unilateral facial nerve crush, transection with amputation of nerve branches, or sham operation. Other group of unlesioned rats received a daily functional electrical stimulation in the levator labii superioris muscle (1 mA, 30 Hz, square wave) or systemic corticosterone (10 mgkg-1). Animals were sacrificed seven days later.Crush and transection lesions promoted no changes in the number of neurons but increased the neurofilament in the neuronal neuropil of axotomized facial nuclei. Axotomy also elevated the number of GFAP astrocytes (143% after crush; 277% after transection) and nuclear FGF-2 (57% after transection) in astrocytes (confirmed by two-color immunoperoxidase) in the ipsilateral facial nucleus. Image analysis reveled that a seven days functional electrical stimulation or corticosterone led to elevations of FGF-2 in the cytoplasm of neurons and in the nucleus of reactive astrocytes, respectively, without astrocytic reaction.FGF-2 may exert paracrine/autocrine trophic actions in the facial nucleus and may be relevant as a therapeutic target to Bell's palsy.It is important the knowledge on the molecules involved in the trophic mechanisms of motoneurons in order to develop therapeutic targets to peripheral nerve disorders which are the case of facial nerve in the Bell's palsy. The disease usually does not last long and undergoes spontaneous recovery in many cases but sometimes therapeutic interventions are necessary to reduce the symptoms or when amelioration is not achieved.In the disorder, the compromised facial nerve swells up and presses against its trajectory inside the temporal bone, being squashed and functionally/anatomically impaired [1]. Around one in five people will suffer long lasting symptoms. In patients presenting incomplete facial palsy and probably bearing only functional impairments, the prognosis for recovery is very good and treatment may be unnecessary. On the other hand, patients presenting complete paralysis, marked
%U http://www.jbppni.com/content/5/1/16