Connectivity of ectopic neurons in the molecular layer of the somatosensory cortex in autoimmune mice

Approximately 50% of New Zealand Black mice (NZB/BINJ) and 80% of NXSM-D/Ei J mice prenatally develop neocortical layer I ectopias, mostly in somatosen sory cortices. These cortical anomalies are similar to those seen in the br ains of individuals with dyslexia. Neurofilament staining revealed a radial column of tightly packed fiber bundles in the layers underlying ectopias. This suggested that the connectivity of the ectopic neurons was aberrant. T he present study used the tracers 1,1'-dioctadecyl- 3,3,3',3'-tetramethylin docarbocyanine perchlorate (Dil) and biotinylated dextran amine (BDA) to mo re thoroughly explore the cortical and thalamic connectivity of the ectopia s. Dil placement into ectopias again revealed a distinct bundle of fibers e xtending from the ectopic neurons to the deep cortical layers. This bundle split in the white matter with some fibers traveling to the corpus callosum and others to the internal capsule. Thalamic connections were concentrated in the ventrobasal complex (VB) and posterior thalamic nucleus group (Po). Injections of BBA into VB revealed reciprocal connections between VB and t he ectopic cortical neurons. Ipsilateral corticocortical projections were s een between ectopias in primary somatosensory and motor and secondary somat osensory cortices, but no contralateral connections of the ectopic neurons were seen. These findings confirm the notion that layer I ectopias are anom alously connected by comparison to neurons in homologous cortex, which may underlie widespread dysfunction of brains containing ectopias.