Abstract

Neonatal freeze lesions to the cortical plate result in focal malformations of the cerebral cortex that resemble four-layered microgyria. These malformations have been associated with local and distant changes in neuronal architecture, and have been implicated in the neocortical epileptiform discharges that can spread up to 4 mm away from the malformation itself. In an effort to assess potential changes in the development of one population of inhibitory interneurons in this malformation, we measured the density of parvalbumin-immunoreactive (ParvIR) neurons in microgyric and control cerebral cortex on postnatal days 13, 15, 21 and 64. In comparison to controls, microgyric animals exhibited a transient decrease in the expression of parvalbumin immunoreactivity in supragranular neurons, both within the malformation itself and in normal six-layered cortex up to 2 mm adjacent to it. This difference disappeared by P21. In addition, there was a permanent diminution of the density of ParvIR neurons in infragranular layers both within and immediately adjacent to the microgyrus. These results indicate that early injury to the cortical plate gives rise to both focal and more widespread changes in cortical architecture.