Motoneurons of the neonate rat respond to proximal axonal injury with morphological and functional changes and
ultimately with neuronal death. Recent studies showed that both Glial Cell line derived growth factor (GDNF) and
Brain derived neurotrophic factor (BDNF) reduce induced degeneration of motoneurons after axotomy and
avulsion. Whether or not rescued motoneurons are functionally intact has been argued. In this present investigation
we will use a proximal crush lesion of the brachial plexus in neonatal rats as the experimental model of neuronal
injury. This will allow us to study the effects of trophic factor administration on injured motoneurons as well as the
relationship between motoneuron survival and extremity function. The number of surviving motoneurons will be
determined by retrograde tracer techniques using horseradish peroxidase (HRP) and Fluorogold (FG). Extremity
function will be quantitatively evaluated with a new behavioral test from day 21 every fourth day until day 42. If
these experiments should demonstrate that enhanced motoneuron survival may lead to improved voluntary function
as the animal enters adulthood, exogenous trophic support of motorneurons might have a role in the treatment of all
types of severe neonatal plexopathies, maintaining the viability of motorneurons until reconstructive surgery
provides them with a pathway for regeneration and endogenous trophic support.