Histometric changes and cell death in the thalamus after neonatal neocortical injury in the rat.
Freezing injury to the developing cortical plate results in a neocortical malformation resembling four-layered microgyria. Previous work has demonstrated that following freezing injury to the somatosensory cortex, males (but not females) have more small and fewer large cells in the medial geniculate nucleus. In the first experiment, we examined the effects of induced microgyria to the somatosensory cortex on neuronal numbers, neuronal size, and nuclear volume of three sensory nuclei: ventrobasal complex, dorsal lateral geniculate nucleus, and medial geniculate nucleus. We found that there was a decrease in neuronal number and nuclear volume in ventrobasal complex of microgyric rats when compared with shams, whereas there were no differences in these variables in the dorsal lateral geniculate nucleus or medial geniculate nucleus. We also found that there were more small and fewer large neurons in both ventrobasal complex and medial geniculate nucleus. In experiment 2, we attempted to determine the role of cell death in the thalamus on these histometric measures. We found that cell death peaked within 24 h of the freezing injury and was concentrated mostly in ventrobasal complex. In addition, there was evidence of greater cell death in males at this age. Taken together, these results support the notion that males are more severely affected by early injury to the cerebral cortex than females.
Rosen
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GD
Dyslexia Research Laboratory and Charles A. Dana Research Institute, Department of Neurology, Division of Behavioral Neurology, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA; Harvard Medical School, Boston, MA 02115, USA. Electronic address: grosen@bidmc.harvard.edu.
Mesples
B
B
Dyslexia Research Laboratory and Charles A. Dana Research Institute, Department of Neurology, Division of Behavioral Neurology, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA; Harvard Medical School, Boston, MA 02115, USA.
Hendriks
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M
Dyslexia Research Laboratory and Charles A. Dana Research Institute, Department of Neurology, Division of Behavioral Neurology, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA; Harvard Medical School, Boston, MA 02115, USA.
Galaburda
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AM
Dyslexia Research Laboratory and Charles A. Dana Research Institute, Department of Neurology, Division of Behavioral Neurology, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA; Harvard Medical School, Boston, MA 02115, USA.
D000367:Age Factors; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D001930:Brain Injuries / Q000473:pathology*; D001931:Brain Mapping; D002452:Cell Count / Q000379:methods; D016923:Cell Death / Q000502:physiology; D048429:Cell Size; D005260:Female; D005452:Fluoresceins; D005615:Freezing; D020287:In Situ Nick-End Labeling / Q000379:methods; D008297:Male; D019579:Neocortex / Q000473:pathology* / Q000503:physiopathology; D009474:Neurons / Q000473:pathology*; D009930:Organic Chemicals; D011247:Pregnancy; D011897:Random Allocation; D051381:Rats; D012737:Sex Factors; D013788:Thalamus / Q000473:pathology*; D013997:Time Factors
D005452:Fluoresceins; D009930:Organic Chemicals; C435731:fluoro jade