USE-DEPENDENT GROWTH OF PYRAMIDAL NEURONS AFTER NEOCORTICAL DAMAGE

Unilateral damage to the forelimb representation area of the sensorimo tor cortex in adult rats increases dendritic arborization of layer V p yramidal neurons of the contralateral homotopic cortex. Arbor size was maximum at approximately 18 d postlesion, following which there was a partial elimination, or pruning, of dendritic processes. These neural changes were closely associated with behavioral events. The overgrowt h of dendrites was related in time to disuse of the contralateral(to t he lesion) forelimb and over-reliance on the ipsilateral forelimb for postural and exploratory movements. The pruning of dendrites was relat ed to a return to more symmetrical use of the forelimbs. To investigat e the possibility that lesion-induced asymmetries in motor behavior co ntributed to dendritic arborization changes, movements of the forelimb ipsilateral to the lesion were restricted during the period of dendri tic overgrowth through the use of one-holed vests. This interfered wit h the increase in dendritic arborization. In contrast, animals that we re allowed to use both forelimbs, or only the forelimb ipsilateral to the lesion, showed the expected increases. When sham-operated rats wer e forced to use only one forelimb, no significant increases in arboriz ation were found. Therefore, neither a lesion nor asymmetrical limb us e alone could account for the dendritic overgrowth-it depended on a le sion-behavior interaction. Furthermore, greater sensorimotor impairmen ts were found when the dendritic growth was blocked, suggesting that t he neural growth and/or associated limb-use behavior were related to f unctional recovery from the cortical damage. Finally, in a second expe riment, immobilization of the impaired limb during the pruning period did not prevent the elimination of processes. Thus, the pruning of neu ral processes was not related simply to the recovery of more symmetric al forelimb use. There may be a period early after brain damage during which marked neural structural changes can occur in the presence of a dequate behavioral demand.