Role of residual anterior neocortex in recovery from neonatal prefrontal lesions in the rat.
Lesions of mediofrontal cortex in adult rats produce behavioral impairments on spatial alternation tasks as well as retrograde degeneration in the mediodorsal thalamic nucleus. The severity of the behavioral deficits and of the thalamic degeneration correlates positively with lesion size. In contrast, similar lesions in neonatal rats (10 days or younger) produce neither spatial alternation deficits nor thalamic degeneration, even after extensive lesions removing all of the mediofrontal cortex. This study examined the possibility that residual anterior cortex remaining intact after early mediofrontal lesions might be involved in the observed anatomical and behavioral sparing. The results show that the sparing of spatial alternation after neonatal frontal cortex lesions does not depend on functional substitution by intact regions of anterior cortex. Neonatal rats receiving extensive lesions including both the medial and orbital frontal cortex or the entire anterior neocortex remained unimpaired on this task. However, these same animals suffered severe retrograde degeneration in the mediodorsal thalamus. Therefore, although some form of neural plasticity cannot be entirely dismissed as the basis for the behavioral results, it seems more likely that behavioral rather than neural plasticity is involved. We suggest that rats deprived of frontal cortex from infancy are able to perform the spatial alternation task in a manner that differs from that used by most intact rats.
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D005260:Female; D005625:Frontal Lobe / Q000293:injuries* / Q000503:physiopathology; D007858:Learning / Q000502:physiology*; D008297:Male; D009473:Neuronal Plasticity; D051381:Rats; D012153:Retention, Psychology / Q000502:physiology; D013787:Thalamic Nuclei / Q000473:pathology / Q000503:physiopathology; D014163:Transfer, Psychology