In the literature that continuous exposure to learning tasks

Irradiation did not impact this group��s ability to learn to distinguish a novel odor from a familiar odor, as was evident by the lack of an effect of x-irradiation on Day 1 DI��. While acute 2 Gy X-ray exposures, like those in the present study, have been shown to significantly decrease the numbers of proliferating cells and immature neurons in the brains of rodents, there are also suggestions in the literature that continuous exposure to learning tasks such as the ID procedure may act to provide an ��enriched environment�� that stimulates neurogenesis following irradiation, thus possibly reducing potential cognitive deficits. Fan and colleagues demonstrated the positive effect of environmental enrichment on brain irradiation and neurogenesis following an acute exposure to 10 Gy X-rays, a dose much higher than the 2.3 Gy dose used in the current study; ��enriched�� animals displayed significant increases in neurogenesis following radiation and decreased cognitive deficits. Such an interpretation agrees with the subtle effects of X-irradiation effects on the ID task, which was assessed first following irradiation, and also with the lack of significant effects of radiation on the social recognition Rhoifolin memory task that was completed following the conclusion of the possibly enriching ID testing. While the tasks used in the current study are not thought to explicitly require the hippocampus, there is evidence in the literature regarding the interaction of the hippocampus with numerous areas of the brain involved in performance of these tasks, including the medial prefrontal cortex, basal Nardosinone forebrain, both anterior and posterior cingulate cortices, and the perirhinal cortex. For example, afferent and efferent pathways connect the hippocampus to the medial prefrontal cortex, and while damage alone to this area could impact simple discrimination, the fact that these areas are part of an interconnected network suggests that damage to either area could cause deficits in attentional set shifting. Indeed, hippocampal neurogenesis has been shown to play a role in cognitive flexibility in mice, the same cognitive domain assessed in the ID task used in the present study.