NMDA receptor antagonists impair memory for nonspatial, socially transmitted food preference.

Roberts, Michael; Shapiro, Matthew L.

doi:10.1037/0735-7044.116.6.1059

Cited by 25 publications

(14 citation statements)

References 60 publications

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“…Training in the STFP task results, in young rats, in phosphorylation of CREB in the hippocampus ). Memory in this task is sensitive to damage of several brain regions, including the hippocampus (Winocur and Moscovitch 1999;Alvarez et al 2002;Clark et al 2002;Roberts and Shapiro 2002;Ross and Eichenbaum 2006). Interestingly, hippocampal lesions prior to training lead to rapid forgetting in this task (Winocur 1990;Bunsey and Eichenbaum 1995;Winocur et al 2001).…”

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confidence: 99%

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

Countryman¹,

Gold²

2007

Learn. Mem.

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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;

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confidence: 99%

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

Countryman¹,

Gold²

2007

Learn. Mem.

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“…For instance, systemic and intra-amygdalar administration of N-methyl-D-aspartate receptor (NMDAr) antagonists such as MK-801 or 2-amino-5-phosphonovaleric acid (APV) have been shown to impair fear acquisition in adult, juvenile, and infant rats (Miserendino et al 1990;Fanselow and Kim 1994;Rodrigues et al 2001;Langton et al 2007;Laurent and Westbrook 2009). NMDArs have also been shown to be important for other learning tasks such as spatial learning (Butelman 1989;Morris 1989), object recognition (de Lima et al 2005), the social transmission of food preferences (Roberts and Shapiro 2002), and eyeblink conditioning (Takatsuki et al 2001).…”

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confidence: 99%

Traces of memory: Reacquisition of fear following forgetting is NMDAr-independent

Richardson

2013

Learn. Mem.

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Recent research shows that while initial learning is dependent on N-methyl-D-aspartate receptors (NMDArs), relearning can be NMDAr-independent. In the present study we examined whether this switch also occurs following forgetting. The developing animal exhibits much more rapid rates of forgetting than adults, so infant rats were used. It was found that infant rats required NMDArs to learn fear (Experiment 1), and that this memory was forgotten after 14 d (Experiment 2). Despite forgetting, relearning fear did not require NMDAr activation (Experiment 3), even if it occurred in adulthood (Experiment 5). Importantly, animals only showed NMDAr-independent reacquisition if they had received paired (white noise–shock) training during conditioning and not if they received unpaired presentations of the white noise and shock (Experiment 4). In addition, this transition following forgetting was not stimulus specific as learning about a novel stimulus (i.e., light, Experiment 6) was also NMDAr-independent. However, reacquisition to a novel stimulus was NMDAr-dependent if the original fear memory was retained at the time of retraining (Experiment 7). Taken together, these results demonstrate how fear memories acquired early in life can have a long-lasting impact on later learning, even when they have been apparently forgotten (i.e., they are not expressed in the animal’s overt behavior). Further, they support the idea that while memories may be forgotten, they are not gone.

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“…However, AVP and OT do not improve STFP under all circumstances. Intrahippocampal injections of AVP produced amnesic effects similar to CPP and MK801 as described above (Roberts and Shapiro, 2002). Furthermore, pretest peripheral administration of an AVP metabolite (peptide sequence 4-9) improved subsequent STFP memory at intervals when memory was poor in controls, but it impaired STFP at intervals in which controls showed normal memory (Strupp et al, 1990).…”

Section: Neurotransmitters Neuropeptides and Social Learningmentioning

confidence: 81%

“…The NMDA receptor is yet another target for memory modulation. Rats that received the NMDA receptor antagonists CPP or MK801 showed intact STFP at 24 h but were impaired at 72 h (Roberts and Shapiro, 2002).…”

Section: Neurotransmitters Neuropeptides and Social Learningmentioning

confidence: 99%

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

Kooij

Sandi

2012

Neuroscience & Biobehavioral Reviews

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a b s t r a c tIntact social memory forms the basis of meaningful interactions between individuals. Many factors can modulate the quality of social memory, and these have been studied in detail in rodents. Social memory, however, cannot be considered a single entity. The term social memory reflects different processes, such as social recognition of a novel conspecific individual and social learning (or 'learning from others'). This review summarizes the findings obtained with behavioral paradigms that were developed for the study of memory formation by social recognition and social learning. In particular, we focus on studies that include tests for social habituation/discrimination paradigms, tests for memory of a previously established social hierarchy and the social transmission of the food preference test. The role of individual differences and the main neurobiological mechanisms (i.e., the brain regions and neurochemical systems involved) that have been implicated in each of these types of social-related memories are reviewed. In addition, we address the key modulatory influence of stress on the formation of these types of memories; discussing the contribution of central (corticotropin-releasing factor, CRF) and peripheral (glucocorticoids) stress systems and their interactions with the social neuropeptide systems. Overall, we present here a general overview of the current state of a thriving research area within the field of social neuroscience.

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NMDA receptor antagonists impair memory for nonspatial, socially transmitted food preference.

Cited by 25 publications

References 60 publications

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

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

Traces of memory: Reacquisition of fear following forgetting is NMDAr-independent

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

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