Abstract
BackgroundThe etiology of Bell's palsy can vary but anterograde axonal degeneration may delay spontaneous functional recovery leading the necessity of therapeutic interventions. Corticotherapy and/or complementary rehabilitation interventions have been employed. Thus the natural history of the disease reports to a neurotrophic resistance of adult facial motoneurons leading a favorable evolution however the related molecular mechanisms that might be therapeutically addressed in the resistant cases are not known. Fibroblast growth factor-2 (FGF-2) pathway signaling is a potential candidate for therapeutic development because its role on wound repair and autocrine/paracrine trophic mechanisms in the lesioned nervous system.MethodsAdult 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.ResultsCrush 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.ConclusionFGF-2 may exert paracrine/autocrine trophic actions in the facial nucleus and may be relevant as a therapeutic target to Bell's palsy.
Highlights
The etiology of Bell’s palsy can vary but anterograde axonal degeneration may delay spontaneous functional recovery leading the necessity of therapeutic interventions
We have examined the effects of systemic corticosterone and functional electrical stimulation applied in a facial muscle on Fibroblast growth factor (FGF)-2 expression in non axotomized facial nuclei
Despites facial nerve crush and transection have promoted no changes in the number of the Fibroblast growth factor-2 (FGF-2) immunoreactivity of neuronal profiles in the lesioned side (Figure 1B), the intensity of the FGF-2 immunoreactivity increased slightly in the cytoplasm of neuronal profiles seven days after the axotomy as evaluated qualitatively by means of a direct microscopic analysis (Figure 2A-D)
Summary
The etiology of Bell’s palsy can vary but anterograde axonal degeneration may delay spontaneous functional recovery leading the necessity of therapeutic interventions. Fibroblast growth factor-2 (FGF-2) pathway signaling is a potential candidate for therapeutic development because its role on wound repair and autocrine/paracrine trophic mechanisms in the lesioned nervous system 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. Patients presenting complete paralysis, marked by an inability to close the eyes and mouth on the involved side, that received early treatment might show a favorable response by 3-12 months [2] This indicated that injured facial neurons can be rescued and might undergo regeneration, a process that takes time considering the distance to facial muscle targets. Some cases are resistant to current proposed treatments which are mainly based on antiinflammatory drugs and local neuromuscular manipulations [3]
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