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Effect of aging and prefrontal cholinergic deafferentation on working memory for familiar and novel odors.

Carter ES, Newman LA, Mcgaughy J (2009) Effect of aging and prefrontal cholinergic deafferentation on working memory for familiar and novel odors. Neuroscience 2009 Abstracts 879.14/EE124. Society for Neuroscience, Chicago, IL.

Summary: Aging is associated with cholinergic fiber loss in the entorhinal cortex (EC). Previous research has shown that acetylcholine (ACh) in this region mediates memory for novel information (Schon et al., 2005), and cholinergic lesions of the EC in young rats impair memory for novel, but not familiar, stimuli at an odor delayed non-match to sample task (DNMS; McGaughy et al., 2005). Currently, we tested whether age-related cholinergic fiber loss in the medial EC of male rats would be sufficient to produce impairments in memory for novel information during the DNMS task. Half of the aged animals were subjected to cholinergic depletion of medial, prefrontal cortex (pACh-lx) including both prelimbic and anterior cingulate cortex prior to the onset of testing. We hypothesized that this previous damage would result in impairments in memory for familiar items and would prevent improvements in memory shown after repeated exposure to novel items. Additionally the effects of increasing the delay between sample and choice portions of the test and memory for list of items were assessed. The pACh-lx animals were not impaired relative to sham-lx animals at memory for familiar information when there was a minimal delay between the sample and choice. However if a 15 minute delay was introduced between the sample and choice phase, pACh-lx rats performed more poorly than sham-lx rats. This suggests that ACh in the medial, prefrontal cortex is necessary for maintaining representations of familiar stimuli over a delay period. Aged rats showed accuracy impairments during sessions that required encoding of novel samples relative to their own performance at sessions requiring encoding of familiar samples. This impairment was greater on trials that required rats to discriminate the novel sample from a familiar non-match than on trials where all stimuli were novel. Though the extent of cholinergic fiber loss in EC due to aging was highly similar to that produced by infusion of the 192 IgG saporin to the EC of young rats, the severity of the cognitive impairments due to aging was not as great as that produced by lesioning. These data suggest that impact of damage to the cholinergic fibers of EC may vary based on whether the deterioration is gradual or has an acute onset.

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