Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

Previous work has suggested that neural plasticity after brain damage may be mediated by post-injury behavioral experience. Unilateral electrolytic lesions of the forelimb representation area of the rat sensorimotor cortex (FLsmc) produce neuronal growth in the homotopic contralateral motor cortex including increases in dendritic arborization of the layer V pyramidal neurons (Jones & Schallert, 1992), increases in the number of layer V synapses per neuron (Jones, Kleim & Greenough, 1996) and changes in the configuration of these synapses (Jones, 1997). These structural changes appear to be related to lesion-induced changes in the use of the forelimbs. Following the lesions, rats have impairments in the use of the forelimb contralateral to the lesion and a hyper-reliance on the ipsilateral forelimb (Jones & Schallert, 1992). Use of the ipsilateral forelimb has been found to be necessary for the dendritic arborization increases (Jones & Schallert, 1994) and motor skills training, which enhances the function of the ipsilateral forelimb, enhances the synaptogenesis in layer V (Chu et al., 1997). However, peripheral manipulations of intact (sham-operated) animals do not reproduce the effects found as a result of behavioral manipulations after FLsmc lesions, consistent with the possibility that this post-injury neural plasticity is a product of an interaction between central degenerative events and behavioral change.

Two studies are presented which assess interactions between behavioral experience and brain damage. The first experiment addresses the possibility that mild terminal degeneration in the motor cortex in the presence of appropriate behavioral demand is sufficient to cause layer V neurons to undergo dendritic growth. This hypothesis was tested by independently manipulating degeneration of the transcallosal projections to the motor cortex, via corpus callosum transections, and forelimb use, via limb-restricting cast. The second experiment extends this line of inquiry to another brain region, the paramedian lobule (PML) of the cerebellum. The cerebellum has been implicated in the recovery from motor cortex damage (Boyeson & Krobert, 1992; Boyeson et al., 1993) and has been shown to undergo structural changes in intact adult rats in response to complex motor skills training (Black et al., 1990; Kleim et al., ). The purpose of experiment 2 was to assess whether the PML undergoes structural changes following unilateral FLsmc lesions and whether these changes would be altered as a result of post-injury skills training.

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