Callosal agenesis and absence of primary visual cortex induced by prenatal X rays impair navigation's strategy and learning in tasks involving visuo-spatial working but not reference memory in mice.

This study was designed for the identification of possible and distinct abilities for behavioral recovery after prenatal cerebral damage. We adopted an interesting tool for promotion of cell's death. Due to the fact that neuroblastic cells and early postmitotic neurons on the beginning of differentiation are particularly sensible for the promotion of apoptosis, we used a low whole-body dose of X radiation on pregnant female mice on E16 (sixteenth gestational day) to promote damage on specific cerebral areas of the progeny, given that the pattern of cerebral neurogenesis is not homogeneous. The morphological results were previously described by our team. Here we noticed that the recovery of behavioral functions after prenatal damage seems to be related to specific factors of local cortical circuitry organization. The deficits found on visual navigation and working memory contrast with the recovery of primary visual functions and also with reference memory, where the mice have a delay on acquisition of learning but get it. As a conclusion we reasoning that changes on laminar organization on frontal cortex as well as the inter hemispheric cortical integration through the corpus callosum could promote relatively fixed cognitive dysfunctions, as those observed on performances that require strategies for navigation (decision making) and working memory, with consequences also observed on the subsequent learning.