The hypothesis that collateral sprouting might be correlated with recovery of function was tested by a combination of behavioral and anatomical studies. Partial hemisections, sparing the dorsal columns, were made between T l r and L1 of cat spinal cord. Initially, all reflex and locomotor hindlimb activity was depressed ipsilaterally. During two postoperative weeks behavioral and electromyographic responses increased in response to intrinsic reflex elicitation but not to descending or crossed reflex elicitation. Marked improvement in use of the limb occurred as intrinsic reflex activity increased and became, in some cases, hyperactive. The status then remained stable for ten months. Since intrinsic reflexes are mediated by ipsilateral dorsal roots, the intraspinal distribution of L5 or L,; dorsal roots was determined by degeneration methods ten months after hemisection or by quantitative radioautography 20 days after hemisection. By both methods, the dorsal root distribution was found to be asymmetrical in the spinal gray. It was greater on the experimental side and the distribution was altered, having a greater distribution medially in Rexed's lamina VI and laterally in lamina VII. These anatomical changes are considered as signs of collateral sprouting from dorsal roots in response to degeneration of descending tracts on the same side. Dorsal root distribution to dorsal horn (laminae I-IV), motor nuclei, and nucleus gracilis is symmetrical. Regions of increased and of expanded dorsal root input can be correlated with electrophysiologically determined location of interneurons in the path of cutaneous reflexes and of stretch reflex facilitation. Behavioral and anatomical changes were selective; intrinsic reflexes recovered or became hyperactive and ipsilateral dorsal roots showed evidence of collateral sprouting during the recovery period, although a causal relationship between the two cannot be proven, by the present experiments.

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The effects of the gamma-aminobutyric acid (GABA) antagonist bicuculline (BCC) on hindlimb motor performance was examined in mature spinal cats with spinal cord transections made either on the day of birth or at approximately two weeks postpartum and in chronic adult cats with spinal transections made in adulthood. In those adult operates, whose pre-drug performance was poor compared to neonatal operates, treadmill locomotion and weight support were improved dramatically by BCC administration. In neonatal operates (examined as adults), BCC administration increased the force of extension to abnormal levels and this increase appeared to disrupt locomotion. Immunocytochemical localization of GABA's synthetic enzyme, glutamic acid decarboxylase (GAD) within the spinal cords of these animals revealed an abnormal distribution of GAD reaction product only in newborn operates. The behavioral results indicate that the full extent of recovery in adult operates is prevented by inhibitory influences and this may contribute to the comparatively superior performance of neonatal operates i.e., the infant lesion effect. The anatomical results suggest that one requirement for the normal development of some intrinsic spinal circuitry is transneuronal regulation mediated by the maturation of descending systems.

Spinal cord damage in neonatal cats has different effects on different spinal pathways. Corticospinal projections exhibit anatomical plasticity, forming an aberrant pathway that bypasses the lesion. In contrast, brainstem-spinal pathways undergo massive retrograde degeneration. Neither of these responses occurs in adult cats. Sparing of motor function is found in cats operated on as neonates but not in cats operated on as adults, and appears to depend on the plasticity of the corticospinal tract.

No abstract