A BEHAVIORAL-ANALYSIS OF RATS WITH DAMAGE TO THE MEDIAL PREFRONTAL CORTEX USING THE MORRIS WATER MAZE - EVIDENCE FOR BEHAVIORAL FLEXIBILITY, BUT NOT FOR IMPAIRED SPATIAL NAVIGATION

In this study, the functional properties of the medial prefrontal cort ex (mPFC) of the rat were examined in a task for spatial navigation. T he dorsomedial (dmPFC) and ventromedial (vmPFC) parts of the PFC diffe r in their connectivity with the hippocampus, vmPFC being the main rec ipient of hippocampal input. Therefore, it is hypothesised that in a s patial task known to be particularly sensitive to hippocampal, but als o to prefrontal cortical damage, especially vmPFC is committed to prop er spatial learning and memory. Using the Morris water maze task, with an invisible platform, male rats with either partial (dmPFC or vmPFC) or whole (mPFC) bilateral lesions were subjected to various procedure s reflecting spatial learning and memory, including a spatial reversal . Animals with dmPFC, vmPFC and mPFC lesions learned and remembered th e spatial task equally well as their controls, regardless of the size or site of the bilateral lesion. However, when presented with a spatia l reversal, animals with whole mPFC lesions were initially slower in l ocating the invisible platform than controls and animals with partial mPFC damage, but this effect was only short-lasting. When subsequently presented with a visible platform, all animals with partial (dmPFC or vmPFC) or whole mPFC damage needed significantly more time to locate the platform than the controls. This effect was transient and lasted l onger in the animals with whole mPFC damage than in animals with parti al damage. On the basis of these findings we conclude that an intact m PFC is not necessary for proper spatial learning and memory. The impai rments in the reversal task and especially in the visually-cued task c an best be explained as a diminished behavioural flexibility when a sh ift in task demands occurs. Since the degree of this impairment was re lated to the size of these lesions, but not to their sites, these diff erences are ascribed to a 'mass action' of medial prefrontal cortex le sions.