Opposite impacts of tenascin-C and tenascin-R deficiency in mice on the functional outcome of facial nerve repair.

The glycoproteins tenascin-C (TNC) and tenascin-R (TNR) are extracellular matrix proteins involved in the development, plasticity and repair of the nervous system. Altered expression patterns after nerve lesions in adult animals have suggested that these molecules influence axonal regeneration. To test this hypothesis, we investigated adult mice constitutively deficient in the expression of TNC, TNR or both, using the facial nerve injury paradigm.

Factors limiting motor recovery after facial nerve transection in the rat: combined structural and functional analyses.

It is believed that a major reason for the poor functional recovery after peripheral nerve lesion is collateral branching and regrowth of axons to incorrect muscles. Using a facial nerve injury protocol in rats, we previously identified a novel and clinically feasible approach to combat axonal misguidance--the application of neutralizing antibodies against neurotrophic factors to the injured nerve. Here, we investigated whether reduced collateral branching at the lesion site leads to better functional recovery.