Abstract Forty percent of New Zealand Black (NZB) mice, a strain that develops severe autoimmune disease, have ectopic collections of neurons in layer I of the neocortex. This strain is used as a model for similar anomalies seen in the dyslexic brain. In the present study we immunohistochemically stained radial glial fibers and their anchoring processes (which form the glial external limiting membrane) in the region of ectopias in NZB mice. The organization of glial fibers was abnormal in and around the ectopic region. Radial glial fibers underlying the ectopia were denser than in the surrounding cortex, and within the ectopia there was a disorganized matrix of glial fibers. Most glial fibers, however, did not enter the ectopia, but instead curved towards the edge of the ectopia and attached there. The glial limiting membrane was breached in the area of the ectopia, indicating that an insult to this membrane may have allowed neurons to migrate into layer I and the overlying subarachnoid space. This finding along with the results of the accompanying paper on puncture wounds of the cortex of newborn rodents supports the view that rupture of the external limiting glial membrane is responsible for the inappropriate migration of neurons into the molecular layer.