Unilateral induced neocortical malformation and the formation of ipsilateral and contralateral barrel fields.
Freezing lesions to the developing cortical plate of rodents results in a focal malformation resembling human 4-layered microgyria, and this malformation has been shown to result in local and widespread disruptions of neuronal architecture, connectivity, and physiology. Because we had previously demonstrated that microgyria caused disruptions in callosal connections, we hypothesized that freeze lesions to the postero-medial barrel sub-field (PMBSF) in one hemisphere would affect the organization of this barrel field contralaterally. We placed freeze lesions in the presumptive PMBSF of neonatal rats and, in adulthood, assessed the architecture of the ipsilateral and contralateral barrel fields. Malformations in the PMBSF resulted in a substantial decrease in the number of barrels as identified by cytochrome oxidase activity. More importantly, we found an increase in the total area of the contralateral PMBSF, although there was no difference in individual barrel cross-sectional areas, indicating an increase in the area of inter-barrel septae. This increase in the septal area of the contralateral PMBSF is consistent with changes in callosal and/or thalamic connectivity in the contralateral hemisphere. These results are another example of both local and widespread disruption of connectional architecture following induction of focal microgyria.
Rosen
G D
GD
Dyslexia Research Laboratory and Charles A. Dana Research Institute and Department of Neurology, Division of Behavioral Neurology, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215, USA. grosen@caregroup.harvard.edu
Windzio
H
H
Galaburda
A M
AM
D000818:Animals; D004292:Dominance, Cerebral; D003576:Electron Transport Complex IV / Q000378:metabolism; D005615:Freezing; D019579:Neocortex / Q000002:abnormalities* / Q000473:pathology / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D012016:Reference Values; D014738:Vibrissae / Q000502:physiology*
D003576:Electron Transport Complex IV