Mechanisms contributing to sparing of function following neonatal damage to spinal pathways.
When spinal pathways are damaged in newborn animals and their behavior is examined in adulthood, motor function is superior to that seen in animals in which the same lesion was made in adulthood. This is the infant lesion effect. After neonatal sensorimotor cortex ablation, spinal hemisection, or spinal transection, sparing of contact placing is observed; in adults, all three lesions abolish contact placing permanently. The anatomical correlates of the infant lesion effect are different in each case. After neonatal unilateral cortical ablation, an exuberant crossed corticorubral pathway from the other cortex fails to retract (as it does normally), giving the remaining cortex a path for mediating contact placing. After neonatal spinal hemisection, late-developing corticospinal axons take an aberrant course around the lesion and mediate contact placing. After neonatal transection, the spinal inhibitory GABA-ergic system fails to develop to a normal extent. This may result in abnormal enhancement of spinal reflex pathways, especially since some dorsal roots increase their input after that lesion. Thus, a number of factors may influence the outcome of damage to the developing nervous system.
Goldberger
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D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D002415:Cats; D002540:Cerebral Cortex / Q000502:physiology*; D009043:Motor Activity / Q000502:physiology; D009416:Nerve Regeneration; D009473:Neuronal Plasticity; D009474:Neurons / Q000502:physiology; D013116:Spinal Cord / Q000166:cytology / Q000502:physiology*