Rapid forgetting of social transmission of food preferences in aged rats: Relationship to hippocampal CREB activation

Abstract

A major characteristic of age-related changes in memory in rodents is an increase in the rate of forgetting of new information, even when tests given soon after training reveal intact memory. Interference with CREB functions similarly results in rapid decay of memory. Using quantitative immunocytochemistry, the present experiment examined the number of CREB-and pCREB-immunoreactive neurons in three regions of the dorsal and ventral hippocampus (dentate gyrus, CA3, and CA1) as a function of age and training. Rats were trained in a social transmission of food preference task. Using different food pairings, memory was tested in each rat immediately and 1, 2, 3, and 7 d later. Both young and old rats had intact and comparable memory scores at the immediate and 24-h tests, but old rats exhibited more rapid forgetting thereafter relative to that of young rats. The main findings were that training resulted in large increases in the number of pCREB-immunoreactive cells throughout the hippocampus in both young and aged rats. However, particularly in the ventral hippocampus, the training-elicited increase in pCREB-positive neurons was significantly lower in old than in young rats. Based on Western blot analyses in a separate set of rats, CREB levels were not responsive to training but were lower in the ventral hippocampus of old rats than of young rats. The present findings suggest that lower activation of CREB after training may contribute to the rapid forgetting seen in aged rats.Rats and mice exhibit age-related impairments in learning and memory on many tasks. Often, the impairments can be characterized in terms of rapid forgetting, in which aged rats and mice have relatively comparable learning and memory on tests soon after training, but poor memory at later times after training (Barnes and McNaughton 1985;

BDNF is essential to promote persistence of long-term memory storage

“…Importantly, the present findings may bridge the concepts of cellular consolidation developed by McGaugh (2) and extensively studied over the years by his group and by many others (18,22,23), including ours (6,17,19,29,39), and that of systems consolidation, originally posited by Squire and his collaborators (40-44). Squire and his associates produced substantial evidence that there is a consolidation process that may last for weeks in rodents and for years in humans (40).…”

“…In addition, deficits in BDNF and in ERK signaling are associated to memory impairment in the aging brain (35,36). Age-related memory impairments have often been characterized in terms of rapid forgetting, in which aged animals have relatively comparable learning and memory on tests performed 24-48 h after training, but poor LTM retention at later times (6). Unraveling the molecular mechanisms involved in memory persistence may help to understand and treat the deficits in memory storage associated with normal and pathological aging.…”

“…LTM requires, whereas STM does not, a gene expression and protein synthesis-dependent stabilization process named consolidation that takes place in restricted areas of the brain, particularly in the hippocampus (1)(2)(3). Depending on the strength and/or saliency of the information to be remembered, consolidated LTMs can persist for just 24-48 h or for many days or weeks (4)(5)(6). For LTM to become long-lasting, changes must persist after acquisition to render the trace immune to molecular turnover (1,2,7).…”

Social memories in rodents: Methods, mechanisms and modulation by stress

“…For example, old (24-month-old) Wistar rats typically demonstrate reduced social recognition in juvenile compared to young (3-month-old) rats (Prediger et al, 2006). Similarly, memory retention in the STFP test with test delays exceeding 24 h was impaired in old (32-month-old) rats compared to young (3-month-old) subjects (Countryman and Gold, 2007). Interestingly, the memory impairments in the STFP test in aged rats were associated with decreased pCREB, notably in the ventral hippocampus (see also Section 4.2.1) (Countryman and Gold, 2007).…”

Hyponeophagia: A Measure of Anxiety in the Mouse

“…It has been suggested that the neocortical cholinergic system, particularly the orbitofrontal component 19 may be more important than the hippocampal cholinergic system for social transmission. Social transmission has even been shown to track memory impairment in aged rats, probably mediated by decreased CREB (cAMP-response element-binding protein) transmission in the aged hippocampus 7 .…”