Neonatal motor cortex lesions in the rat: Absence of sparing of motor behaviors and impaired spatial learning concurrent with abnormal cerebral morphogenesis.

Abstract

Rats with removal of the motor cortex in adulthood were compared behaviorally and neuroanatomically with rats with similar removals at 4 days of age. The results suggest that neonatal ablation of the motor cortex of rats is more debilitating behaviorally than similar injury in adulthood and produces abnormal morphogenesis of the posterior neocortex. Neonatal lesions of the motor cortex produced more chronic abnormalities in movements of the distal effectors that accompany adult lesions (tongue, snout, and digit use) and, in addition, produced abnormalities in limb placement on a narrow beam and a significant impairment in spatial learning, neither of which is associated with adult lesions. When the brains of neonatally operated rats were compared with those of control rats or rats operated on in adulthood, there were striking differences. Although the area of cavity appeared smaller in the neonatal operates, their brains weighed less, the neocortex was thinner, and the cross-sectional area of the remaining cortex was reduced, when compared with those of the adult-operated group. It is suggested that studies of the acquisition of various neuropsychological learning tasks may have greatly overestimated the degree of sparing following anterior neocortical lesions in rats.

Thinning, movement, and volume loss of residual cortical tissue occurs after stroke in the adult rat as identified by histological and magnetic resonance imaging analysis

“…The results of the present study are similar to those found after neonatal cortical stroke (Kolb and Holmes, 1983) and adds to current literature by describing the temporal and spatial progression of post-stroke cortical thinning in adult rat models. Additionally, by utilizing MRI, the present study is the first to confirm this morphological progression in vivo in an animal model and, to our knowledge, is the first to quantify the extent of residual tissue movement into the stroke infarct.…”

“…First, it has been suggested that cortex can thin by moving into the infarct cavity. This would be especially notable in the pial strip model in which tissue can move into not only the infarct, but also into the cavity produced by the trephination itself (Adams et al, 1994;Kolb & Holmes, 1983;Navari et al, 1978;Whishaw, 2000;Xu et al, 2007). Second, all of the stroke models likely involve neuroinflammatory responses, secondary neurodegeneration, and apoptosis, which take place over time following the stroke (Chen et al, 2003;Bidmon et al, 1998;Pulsinelli, 1982;Witte et al, 2000).…”

“…Neuronal migration is known to continue well into the first week of life in the rat (Bayer and Altman, 1991;Hicks and D'Amato, 1968) and it has previously been reported that migration is disrupted after small cortical lesions in the neonatal rat (Hicks and D'Amato, 1968). Kolb and colleagues (Kolb and Holmes, 1983;Kolb and Whishaw, 1985), document in many of their studies that the size of the stroke infarct appears much smaller in neonatal operates compared to adult operates, despite their best efforts to standardize stroke size across all groups. One possible explanation is that the stroke core was filled with newborn neurons after the stroke, which indeed occurs after P10, but not P1 or adult stroke .…”

“…Some studies make comparisons to tissue in a non-stroke control animal, whereas others use the intact contralateral hemisphere within the same stroke animal. Finally, age may be a contributing factor as stroke in infant subjects produces extensive gross morphological changes in remaining tissue including thinning, movement, and filling in of the stroke infarct (Kolb and Whishaw, 1981;Kolb and Holmes 1983;Kolb et al, 1983aKolb et al, ,b, 1987Kolb 1987;Whishaw, 2000;Alaverdashvili and Whishaw, 2010). In short, the complexity of these morphological changes makes it difficult to make comparisons between homologous cortical regions in intact control rats and stroke rats.…”

Metabolic Maturation of the Brain: A Study of Local Cerebral Glucose Utilization in the Developing Cat

“…The kitten's brain matures faster, such that at 3 weeks of age it is comparable to that of a baby born at term. By comparison, nonhuman primates are born relatively more mature (Passing ham et aI., 1983) whereas the brain of the rat is considerably less mature at birth (Kolb and Holmes, 1983;Almli, 1984). (ii) The cat is an ad vanced mammal with a rich and extensively studied behavioral repertoire (see Olm stead, 1979, 1982) and thus allows for metabolic behavioral correlations.…”