Induction of molecular layer ectopias by puncture wounds in newborn rats and mice.
Molecular layer ectopias spontaneously occur in immune-disordered mice, and the accompanying paper demonstrates that these ectopias are associated with a break in the external glial limiting membrane and with distortion of radial glial fibers at birth. It was hypothesized that injury to the developing neocortex is the main etiologic event for molecular layer ectopias. To test this hypothesis, puncture wounds were made on the surface of the cerebral cortex of newborn rats and mice. These wounds produced, in adulthood, molecular layer ectopias similar in appearance to those seen spontaneously in immune-disordered mice. Further, these ectopias show similar distortions of radial glial fibers during development, and of neurofilaments in adulthood. This work supports the notion that injury could be a factor in the production of molecular layer ectopias.
Rosen
G D
GD
Dyslexia Research Laboratory, Beth Israel Hospital, Boston, MA 02215.
Sherman
G F
GF
Richman
J M
JM
Stone
L V
LV
Galaburda
A M
AM
D000375:Aging; D000818:Animals; D000831:Animals, Newborn; D001930:Brain Injuries / Q000473:pathology*; D002540:Cerebral Cortex / Q000254:growth & development / Q000473:pathology*; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D007124:Immunoenzyme Techniques; D007150:Immunohistochemistry; D007382:Intermediate Filaments / Q000648:ultrastructure; D051379:Mice; D008811:Mice, Inbred DBA; D051381:Rats; D011919:Rats, Inbred Strains; D013194:Staining and Labeling; D014746:Vimentin / Q000032:analysis; D014951:Wounds, Stab / Q000473:pathology*
D005904:Glial Fibrillary Acidic Protein; D014746:Vimentin