Denervation facilitates neuronal growth in the motor cortex of rats in the presence of behavioral demand.

This study tests the hypothesis that degeneration of a neocortical pathway may facilitate behaviorally-induced growth of neurons in a connected region of the cortex. Degeneration of trancallosal afferents to the motor cortex and changes in forelimb use were independently manipulated in adult rats. The combination of degeneration and behavioral change resulted in the growth of layer V pyramidal neuron dendrites which was not found as a result of either denervation or behavioral manipulation alone. These results indicate that mild degeneration in the adult brain can facilitate neuronal growth when accompanied by appropriate behavioral demand, a finding which has implications for rehabilitative therapy after brain damage.

Reactive astrocytic responses to denervation in the motor cortex of adult rats are sensitive to manipulations of behavioral experience.

Recent research has suggested that mild denervation of the neocortex of adult rats may facilitate neuronal growth in response to behavioral changes. Astrocytes react to denervation, produce growth-promoting factors and are a potential mediator of this denervation-facilitated growth. The present study assessed whether astrocytic reactions to denervation vary dependent upon post-injury behavioral experience. Denervation of the transcallosal afferents to the motor cortex was induced via partial transections of the corpus callosum. Transected- or sham-operated rats were then either forced to use the opposite forelimb (via limb-restricting vests) or permitted to use both forelimbs normally for 8 days. In the motor cortex, the surface density of glial fibrillary acidic protein (GFAP)-immunoreactive (IR) astrocytic processes and the density of basic fibroblast growth factor (FGF-2)-IR glial cells was significantly increased as a result of transections alone and as a result of forced forelimb-use alone in comparison to controls. The combination of transections and forced-use significantly enhanced GFAP-IR in comparison to all other groups, but did not further enhance FGF-2-IR. These findings are consistent with behavior and denervation having interactive influences on astrocytic reactivity in the motor cortex. These results also raise the possibility that astrocyte-mediated support of neural restructuring after brain injury might be enhanced with appropriate post-injury behavioral manipulations.