title: Morphological changes in the thalamus and neocortex of the cat brain after a restricted unilateral fetal neocortical lesion.
abstract: In order to study the response of the brain to injury during early development, the neocortex of ten fetal kittens was lesioned at age E43-48, in either the frontal (n = 8) or parieto-occipital (n = 2) areas. The thalamus and neocortex of the lesioned animals were analyzed using quantitative morphometry and compared to intact control cats (n = 10). Ipsilaterally, the volumes of the remaining neocortex and of the thalamus were 26.5% and 25.7% smaller, respectively (P < 0.05). Contralaterally, the neocortex did not change in volume, whereas the thalamus tended to be smaller by a mean of 11.1%. Ipsilaterally, in all four thalamic nuclei studied, the neuronal and glial cell packing densities (NCPD and GCPD) and the cross sectional area of neuronal somata did not differ between lesioned and intact animals except for the principal ventromedial nucleus, where the GCPD was significantly lower (P < 0.05) in lesioned animals. Contralaterally, the NCPD and GCPD did not show any differences between groups, except for the principal ventromedial nucleus, in which the GCPD was lower in lesioned cats (P < 0.05). Furthermore, in the contralateral basal ventromedial nucleus, the cross sectional area of the neuronal somata was smaller in lesioned than in intact animals (P < 0.01). These results indicate loss of neurons and glia in the ipsilateral thalamus and probably in the neocortex. Since, at the time of the cortical resection, transient reciprocal thalamosubplate connections have been established in the cat, the lesion-induced deprivation of subplate target neurons and cortical inputs probably precluded the survival of a substantial number of developing thalamic neurons. In the cortex the hypothetical loss of neurons may, at least partly, be attributed to lesion-induced elimination of target neurons before establishment of corticocortical connections.
authors.affiliation: Department of Psychiatry and Biobehavioral Science, UCLA School of Medicine, USA.
authors.forename: L D
authors.initials: LD
authors.lastname: Loopuijt
authors.forename: J R
authors.initials: JR
authors.lastname: Villablanca
authors.forename: D A
authors.initials: DA
authors.lastname: Hovda
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000196:embryology; D002415:Cats; D002452:Cell Count; D016923:Cell Death; D002470:Cell Survival; D002540:Cerebral Cortex / Q000196:embryology / Q000502:physiology*; D005260:Female; D005333:Fetus; D005625:Frontal Lobe / Q000502:physiology; D007839:Functional Laterality / Q000502:physiology*; D008297:Male; D009410:Nerve Degeneration / Q000502:physiology*; D009474:Neurons / Q000166:cytology; D010296:Parietal Lobe / Q000502:physiology; D013788:Thalamus / Q000196:embryology / Q000502:physiology*