Dissociation between memory retention across a delay and pattern separation following medial prefrontal cortex lesions in the touchscreen TUNL task

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• Dissociation between prefrontal cortical and hippocampal contributions to performance of the TUNL task. • Prefrontal cortex lesions result in delay-dependent, but not separation-dependent impairments on TUNL. • Prefrontal cortex lesions result in modest impairments under high interference conditions of TUNL.

The neural structures that support the retention of memories over time has been a subject of intense research in cognitive neuroscience. However, recently much attention has turned to pattern separation, the putative process by which memories are stored as unique representations that are resistant to confusion. It remains unclear, however, to what extent these two processes can be neurally dissociated. The trial-unique delayed nonmatching-to-location (TUNL) task was developed to assess spatial working memory and pattern separation function using trial-unique locations on a touch-sensitive screen (Talpos, McTighe, Dias, Saksida, & Bussey, 2010). Using this task, Talpos et al. (2010) showed that lesions of the hippocampus led to both impairments with a 6 s delay, and impairments in pattern separation. The present study shows that lesions of the medial prefrontal cortex lead to a different pattern of effects: impairment at the same, 6 s delay, but no hint of impairment in pattern separation. In addition, rats with medial prefrontal lesions were more susceptible to interference in this task. When compared with previously published results, these data show that whereas the prefrontal cortex and hippocampus likely interact in the service of working memory across a delay, only the hippocampus and not the medial prefrontal cortex is essential for pattern separation.

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