Amyloid-β alters medial prefrontal cortex encoding of temporal order task.

BackgroundAlzheimer's disease (AD) is a progressive neurodegenerative disorder linked to dementia. Clinical diagnosis of AD occurs in the mid to advanced disease stages when patients exhibit signs of memory loss or dementia. Likewise, in AD experimental models, animals are assessed in the later stages when behavioral phenotypes are discernible.ObjectivesThe goal of the current study was to investigate the encoding of temporal order recognition (TOR) tasks in the medial prefrontal cortex over a chronic duration before and during toxic or non-toxic amyloid-β (Aβ) lesioning (48 days).MethodsThe current study employs in vivo prefrontal cortex recording during TOR tasks to detect changes in putative pyramidal cell firing rates in naïve brains (baseline) and after toxic Aβ25-35 or control Aβ35-25 lesioning.ResultsTOR recognition index scores were positively correlated with putative unit change in firing rate (FR) during old object exploration intervals. Furthermore, the percentage distribution of putative units with increased FR during old object intervals was more than that of recent object intervals. Interestingly, in Aβ25-35 ensembles, the positive correlation between TOR performance and pyramidal FR was lost. In addition, there was a reduction in the percentage of units with increased FR during old object exploration. Interestingly, a positive correlation was observed between putative unit FR and recognition index scores in control Aβ35-25 ensembles.ConclusionsTaken together, our results showed that toxic Aβ lesioning impacts TOR memory encoding by altering ensemble encoding patterns associated with object recognition and discrimination.