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Autoradiographic and axonal degeneration staining techniques were combined in individual animals to study the distribution of corticopontine fibers. In normal animals, forelimb and hindlimb motor cortical projections terminated somatotopically within the ipsilateral pontine nuclei. Sparse crossed projections also displayed a somatotopic pattern. After unilateral sensorimotor cortical lesions in newborn rats, an increase in the crossed corticopontine fibers arising from the opposite unablated motor cortex was observed at maturity. These fibers distributed in a topographic pattern similar to the normal ipsilateral corticopontine pattern; forelimb motor cortical projections terminated rostral to hindlimb motor cortical fibers. The specific distribution of the anomalous fibers suggests that they constitute a functional pathway.

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Cerebral cortical projections from the forelimb motor cortex, as defined by intracortical microstimulation where movements were evoked at low current intensities (less than 15 microA), were examined in normal rats and in adult rats that sustained neonatal hemicerebellectomy. The distribution pattern of cortical efferent projections in normal rats generally appeared more restricted than previously described. This restricted distribution is attributed to the use of WGA/HRP as the axonal tracing method and to the electrophysiological definition of the injection site as the motor cortex. The observed remodeling of the corticobulbar projections, seen after cerebellar lesions in the young, largely confirmed previous reports. Moreover, no alterations in the laterality of distribution in corticospinal projection were found. Aberrant corticospinal projections were sought in an effort to provide an anatomical basis to a previous description of abnormally low-threshold ipsilateral forelimb responses evoked from the motor cortex in adult rats after neonatal cerebellar lesions. This apparent absence of corticospinal tract remodeling after neonatal hemicerebellectomy suggests that the abnormal responses are mediated by the normal corticospinal pathways. This possibility is discussed in terms of an alteration in the spinal circuits that may change the responsiveness of spinal motoneurons to a given pyramidal discharge.