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Local application of extracellular matrix proteins fails to reduce the number of axonal branches after varying reconstructive surgery on rat facial nerve.

PURPOSE: A major reason for the poor functional recovery after peripheral nerve injury is the outgrowth of supernumerary axonal branches at the lesion site. Projecting within several nerve fascicles, the branches of one axon often re-innervate synchronously muscles with antagonis-tic functions and impair any coordinated activity. We hypothetized that accelerated axonal elongation through extracellular matrix proteins fos-tering neurite outgrowth might reduce axonal branching and improve recovery of function. METHODS: In a control group of rats, ramus zygomaticus, ramus buccalis, and ramus marginalis mandibulae of the facial nerve were transected and the stumps labeled with DiI, Fluoro-Gold (FG), and Fast Blue (FB). RESULTS: Neuron counts showed that the zygomatic ramus contained axons of 204 +/- 88 DiI-labeled motoneurons in the dorsal facial subnu-cleus. No perikarya were labeled by 2 or 3 tracers. After transection and suture of the facial nerve trunk, the zygomatic ramus contained axons of 328 +/- 50 motoneurons dispersed throughout the whole facial nucleus. The occurrence of double-labeled (DiI+FG and DiI+FB) motoneu-rons showed that about 30 % of all axons in the zygomatic ramus had a twin branch projecting within the buccal and/or mandibular ramus. CONCLUSIONS: Entubulation of transected facial nerve in a silicone tube containing phosphate buffered saline, collagen type I, laminin, fibronectin, or tenascin did not reduce the portion of double-labeled motoneurons. We conclude that (i) axonal branching follows a rather con-stant pattern regardless of changes in the local microenvironment; (ii) despite their known effect to support neurite outgrowth, all tested extra-cellular matrix proteins do not suppress axonal branching in the rat facial nerve model.