Abstract
To develop a mouse model for measuring facial nerve injury and recovery and to test the hypothesis that overexpression of the antiapoptotic gene, bcl2, enhances recovery of facial nerve function after peripheral crush injury. Prospective analysis of recovery of function after facial nerve crush injury in mice at juvenile (postnatal day 7) and adult (postnatal day 30) ages with blind comparison of wild-type and transgenic bcl2 overexpression littermates at both ages and immunohistologic confirmation of overexpression of bcl2 in facial motoneurons in transgenic animals. Adult wild-type mice demonstrated full recovery of facial nerve function (measured as eye blink and whisker movement) within 3 weeks of injury. Juvenile wild-type mice demonstrated diminished recovery of function. Juvenile transgenic bcl2 overexpression mice demonstrated more rapid and complete recovery of eye blink but not whisker movement in comparison with wild-type littermates. Measurement of facial nerve function in mice after injury is feasible. Enhanced recovery of facial nerve function in adult mice and mice overexpressing bcl2 indicates that preservation of central motoneurons after injury may improve function after peripheral nerve injury.
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