Thalamic connectivity of the primary motor cortex of normal and reeler mutant mice.

Reeler, an autosomal recessive mutation in mice, causes cytoarchitectonic abnormalities of the cerebral cortex, which are characterized by malposition of neurons. Retrograde and anterograde transport of horseradish peroxidase (HRP) was employed to examine the reciprocal connectivity between the hindlimb area of the primary motor cortex (MI) and thalamus of normal and reeler mutant mice. In the normal mouse, most of the cells labelled after HRP injection into the hindlimb area of MI were located in the ventrolateral nucleus, the lateral division of the ventrobasal nucleus, the central lateral, paracentral and central intralaminar nuclei, and the medial division of the posterior complex. HRP reaction product anterogradely transported was also observed in the same nuclei and in the thalamic reticular nucleus. In the reeler mutant mouse, retrogradely labelled neurons and anterogradely labelled terminals were again found in the nuclei referred to above, and the distribution pattern and morphology of HRP-filled neurons were also similar to those of normal controls. The present results suggest therefore that the normal reciprocal connectivity between MI (hindlimb representation) and thalamus is preserved in the reeler mouse. That is to say, dislocated cortical neurons appropriately project to their target nuclei of the thalamus, and conversely, thalamic neurons send their axons precisely to their target cortical areas of the radially disorganized cortex.