PubMed1995
The reeler genetic mutation, occurring spontaneously in mice, affects migration of neuroblasts in the central nervous system at its last stage, causing severe cytoarchitectonic abnormalities in laminated structures, such as the cerebral and cerebellar cortex. In the reeler mouse, corticospinal (CS) neurons are malpositioned in association with the deranged laminar cytoarchitecture. To examine whether CS projections in the reeler mouse and their collaterals terminating with subcortical nuclei are normal or not, 5% biocytin was injected into the sensorimotor cortex of 2-month-old normal and reeler mice. Anterogradely labeled CS fibers of normal and reeler mice exited from the cortex and entered the internal capsule and the cerebral peduncle. They penetrated the basal pontine gray matter as longitudinal pontine fibers and entered the medullary pyramid. They continued caudally as a compact bundle along the ventral surface of the medulla, passed through the pyramidal decussation at the spinomedullary junction and entered the contralateral dorsal funiculus of the spinal cord. Both in normal and reeler mice, collaterals arising from these CS fibers projected to the ipsilateral red nucleus, basal pontine gray matter, inferior olivary complex, and the contralateral gracile nucleus. Thus, in the reeler mouse, the course and termination of CS fibers and their collaterals are identical to their normal counterparts, suggesting that radially malpositioned CS neurons in the sensorimotor cortex project to the subcortical nuclei in a manner similar to normal CS neurons.