Regional age-dependent effects of hemineodecortication upon contralateral neocortical thickness: comparison with other measures of cortical size.
This study investigated age-dependent changes in regional neocortical thickness after hemineodecortication in cats and compared the results to previously reported volumetric and cross-sectional data. Subjects sustained hemineodecortication on postnatal days (P) P10, P30, P60 or in adulthood. Neocortical thickness was quantified at 115 sites along 20 stereotaxic coronal anterior-posterior (AP) planes using defined sites of the main cerebral sulci for the measurements. The analysis established significantly lower thickness values for adult-lesioned as compared to (a) P30, P60 and control groups at AP +14, (b) P30 group at 7 planes along a range of AP +9 to AP +3, and (c) P10 and P60 groups at AP +6. Both the P10 and the P30 groups presented a significantly thicker neocortex than controls at select coronal planes clustering behind AP +10 (parietal and temporal cortices). When analyzed by sulcus, results once again reflected significant advantages for the early-lesioned cats with a significantly thicker cortex found at 4 of the 8 sulci examined. Again, significant advantages were also discovered for early-lesion subjects compared with control cats (splenial, cruciate sulci). Overall, the range of significant effects (from AP +14 to AP 0) and the direction of the means suggested that there was a significant, age-dependent (P10-P60), regional sparing of neocortical thickness with a peak effect occurring at P30. We concluded that: (a) there was a regional sparing/increase of neocortical thickness suggesting that discrete cortical areas are selectively involved in the resistance to structural atrophy following hemineodecortication in young cats (P10-P60) and (b) the global loss of neocortex volume found in our previous study was not apparent using the present thickness measurement. It is suggested that both of these measurements must be taken into account when assessing morphological effects upon the neocortex either in human pathology (i.e. hemispherectomy, intractable epilepsy) or in animal models.
Schmanke
T D
TD
Department of Neuroscience, New York College of Osteopathic Medicine, Old Westbury, NY 11568-8000, USA. tschmank@iris.nyit.edu
Villablanca
J R
JR
D000375:Aging / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn / Q000254:growth & development / Q000502:physiology; D002415:Cats; D002540:Cerebral Cortex / Q000473:pathology* / Q000502:physiology* / Q000503:physiopathology; D003714:Denervation; D019579:Neocortex / Q000473:pathology*; D009473:Neuronal Plasticity