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Re-examination of the plasticity of the corticothalamic projection after unilateral neonatal lesion of the sensorimotor cortex in the rat: a phaseolus vulgaris-leucoagglutinin tracing study.

After unilateral lesion of the sensorimotor cortex in neonatal rats (postnatal days 2-4), the reorganization of the corticothalamic projection originating from the opposite intact sensorimotor cortex was studied. Three months after the lesion, the anterograde tracer phaseolus vulgaris-leucoagglutinin (PHA-L) was injected in the caudal forelimb area (CFA) of the intact opposite sensorimotor cortex to label the corticothalamic axons, in order to establish their trajectory as well as the distribution of their terminal fields in the thalamus. As previously reported, in addition to the standard ipsilateral corticothalamic projection, lesioned rats were characterized also by the presence of a contralateral corticothalamic projection, reaching the decorticate hemithalamus. There is some controversy in literature whether such bilateral corticothalamic projection is present in normal intact rats. On the basis of counts of axons crossing the midline to innervate the hemithalamus contralateral to the cortical injection, the present study provides evidence that the corticothalamic projection is indeed bilateral in normal rats, although the contralateral projection is sparse. Lesioned rats subjected to a similar small size PHA-L injection in the CFA of the intact opposite cortex showed a significantly increased contralateral corticothalamic projection. The number of labeled axons crossing the midline in the thalamus was, on average, five times higher in lesioned rats than in normal rats. It can be concluded that the contralateral corticothalamic projection from the CFA, observed after neonatal lesion of the opposite sensorimotor cortex, is not a novel projection resulting from the lesion, but rather an enhancement and extension of an existing, minor, projection present in normal rats. The enhancement of the crossing corticothalamic projection in lesioned rats is due to an increase of the number of crossing axons in the thalamus rather than to an increase of the degree of branching of the few axons present in control animals.