Plasticity in the rat spinal cord seen in response to lesions to the motor cortex during development but not to lesions in maturity

Abstract

Motor cortical inputs and proprioreceptive muscle afferents largely target the same spinal cord region. This study explored the idea that during development the two inputs interact via an activity-dependent mechanism to produce mature patterns of innervation. In rats, the forelimb motor cortex was ablated unilaterally at either postnatal day 7 (P7), the beginning of corticospinal synaptogenesis in the cervical cord, or at P50. Comparisons were made with sham-operated animals. At P70, muscle afferents from the extensor digitorum communis muscle, contralateral to the lesion, were transganglionically labeled with cholera toxin B-subunit. Lower cervical spinal cord sections were immunostained for cholera toxin B, parvalbumin, and cJun. Our small lesions had no obvious effects upon forelimb function. However, developmental lesions, but not adult lesions, were shown to significantly increase the number of muscle afferent boutons present in the contralateral ventral horn, compared with sham-operated controls. Also, the ratio of parvalbumin-positive neurons contralateral/ipsilateral to the developmental lesion (but not adult lesions) was decreased and the ratio of cJun-positive motoneurons increased. Thus, an early motor cortex lesion resulted in retention of a proportion of muscle afferent synapses to the ventral horn that are known to be lost during normal development. Parvalbumin and cJun are markers of neuronal activity suggesting that spinal circuitry develops permanently altered activity patterns in response to an early cortical lesion, although this plasticity is lost in the mature animal.