Abstract
Age-related memory impairments show a progressive decline across lifespan. Studies have demonstrated equivocal results in biological and behavioral outcomes of aging. Thus, in the present study we examined the novel object recognition task at a delay period that has been shown to be impaired in aged rats of two different strains. Moreover, we used a strain of rats, Fisher 344XBrown Norway, which have published age-related biological changes in the brain. Young (10 month old) and aged (28 month old) rats were tested on a standard novel object recognition task with a 50-minute delay period. The data showed that young and aged rats in the strain we used performed equally well on the novel object recognition task and that both young and old rats demonstrated a righthanded side preference for the novel object. Our data suggested that novel object recognition is not impaired in aged rats although both young and old rats have a demonstrated side preference. Thus, it may be that genetic differences across strains contribute to the equivocal results in behavior, and genetic variance likely influences the course of cognitive aging.
Highlights
Progressive memory decline is a hallmark of the aging process and some impairments are mediated by the medial temporal lobe including the hippocampus [1]
The results demonstrated that long-term potentiation, (LTP) potentiation decreases with age, as well as the NMDA-mediated field excitatory post-synaptic potential, but no change occurs in the AMPA-mediated fEPSP
We chose a strain of rats with known age-related biological changes in the brain [4,5,6,12,25] and a delay period for the novel object recognition task based on studies in which there are age-related deficits in the novel object recognition task [19,26]
Summary
Progressive memory decline is a hallmark of the aging process and some impairments are mediated by the medial temporal lobe including the hippocampus [1]. The neurobiological changes in the aging brain underlying these cognitive alterations have been investigated. It is well documented that significant cell loss in the structures of the medial temporal lobe does not occur with age and does not contribute to the cognitive changes with age [2,3,4,5,6]. Changes in the number of synapses, which are highly labile structures, are responsive to microenvironmental changes in the brain and result in a continual refinement of neuronal circuitry [7,8], may underlie these cognitive changes. It is very likely that subtle changes in the function of synapses contribute to cognitive declines with age
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