Strain-dependent Differences in LTP and Hippocampus-dependent Memory in Inbred Mice

Nguyen, Peter V.; Abel, Ted; Kandel, Eric R.; Bourtchouladze, Rusiko

doi:10.1101/lm.7.3.170

Cited by 225 publications

(237 citation statements)

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“…C57BL/6 mice are known to perform well in hippocampal-dependent behavioral tasks, including T-maze spontaneous alternation (Gerlai, 1998a) and context-dependent fear condi-tioning (Gerlai, 1998b;Paylor et al, 1994). These mice also exhibit excellent hippocampal long-term potentiation measured ex vivo (Nguyen et al, 2000a) or in vivo (Matsuyama et al, 1997). Using this strain, Gerlai et al (1999) demonstrated impaired acquisition of memory in a hippocampal-dependent manner in response to intrahippocampal infusion of a genetically engineered antibody-like protein, an immunoadhesin, that selectively antagonized EphA function (Gerlai et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

“…The authors explained that "the intention is usually to demonstrate a link between neuronal function and behavior." To work toward this goal, Nguyen et al (2000a) analyzed both the behavioral and synaptic function of four inbred mouse strains: C57BL/6J, CBA/J, DBA/2J, and 129 SvEmsϩ ter /J. These investigators found genotype-dependent differences in LTP and in learning performance between the strains.…”

Section: Inbred Strains: Characterization Of Synaptic Plasticity and mentioning

confidence: 99%

“…Mouse strains have been suggested to be highly useful to address such complex questions as the analysis of the mechanisms of learning and memory (Nguyen et al, 2000a;Nguyen and Gerlai, 2002) and other traits relevant for human disease (Phillips et al, 2001). The implicit assumption behind this suggestion is as follows.…”

Section: Introductionmentioning

confidence: 99%

“…Using this strain, Gerlai et al (1999) demonstrated impaired acquisition of memory in a hippocampal-dependent manner in response to intrahippocampal infusion of a genetically engineered antibody-like protein, an immunoadhesin, that selectively antagonized EphA function (Gerlai et al, 1999). Another inbred strain, DBA/2, which is known to be inferior in some hippocampal tasks (Gerlai, 1998a,b;Paylor et al, 1994), as well as hippocampal LTP (Matsuyama et al, 1997;Nguyen et al, 2000a), was also employed. EphA receptor tyrosine kinase activation by intrahippocampal infusion of an agonist immunoadhesin in this strain led to improved behavioral performance in the T-maze and in contextdependent fear conditioning.…”

Section: Introductionmentioning

confidence: 99%

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Hippocampal LTP and memory in mouse strains: Is there evidence for a causal relationship?

Gerlai

2002

Hippocampus

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ABSTRACT:The mechanisms underlying memory are under intense investigation. One of the most promising candidates at the cellular level is long-term potentiation (LTP). Numerous pharmacological and molecular genetic manipulations have led to alteration in both LTP and memory. However, the causal relationship between these phenotypical changes is debated. The problem of causality can be addressed in numerous ways. One suggestion is to investigate natural variation in both LTP and memory performance in mouse strains. If variation in synaptic and behavioral phenomena is found, correlation between these traits may be investigated. The advantages and disadvantages of this approach are discussed. An empirical example using four mouse strains is also presented to highlight some general problems. The following arguments are made. First, multiple electrophysiological and behavioral paradigms with idiosyncratic condition characteristics should be conducted to avoid false-positive findings due to alterations unrelated to memory and its mechanisms. Multiple stimulation and memory protocols may also allow one to study the complexity and multiplicity of processes. Second, analysis of a large number of mouse strains may be needed to avoid false interpretation of results due to spurious gene associations and/or linkage disequilibrium. Third, quantitative genetic analysis using, for example, diallele crosses, may be employed to properly investigate biologically meaningful, i.e., genetic, effects. It is concluded that with the use of additional methods (e.g., QTL analysis, gene expression arrays, and biochemical analysis) providing converging evidence, analysis of mouse strains will be instrumental in addressing the question regarding the role LTP may play in memory. Hippocampus 2002;12:657-666.

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Section: Introductionmentioning

confidence: 99%

Section: Inbred Strains: Characterization Of Synaptic Plasticity and mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Hippocampal LTP and memory in mouse strains: Is there evidence for a causal relationship?

Gerlai

2002

Hippocampus

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“…Although the existence of variation in learning abilities among individuals belonging to the same species has been recognized for a long time (James 1890;Habib et al 2000;Nguyen et al 2000), the neurobiological correlates underlying such variability are largely unknown. In humans, imaging studies have shown different patterns of brain activation to be associated with different levels of learning and memory performance (Habib et al 2000;Cazalis et al 2003).…”

mentioning

confidence: 99%

Neurobiological and Endocrine Correlates of Individual Differences in Spatial Learning Ability

Sandi¹,

Cordero²,

Merino³

et al. 2004

Learn. Mem.

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The polysialylated neural cell adhesion molecule (PSA-NCAM) has been implicated in activity-dependent synaptic remodeling and memory formation. Here, we questioned whether training-induced modulation of PSA-NCAM expression might be related to individual differences in spatial learning abilities. At 12 h posttraining, immunohistochemical analyses revealed a learning-induced up-regulation of PSA-NCAM in the hippocampal dentate gyrus that was related to the spatial learning abilities displayed by rats during training. Specifically, a positive correlation was found between latency to find the platform and subsequent activated PSA levels, indicating that greater induction of polysialylation was observed in rats with the slower acquisition curve. At posttraining times when no learning-associated activation of PSA was observed, no such correlation was found. Further experiments revealed that performance in the massed water maze training is related to a pattern of spatial learning and memory abilities, and to learning-related glucocorticoid responsiveness. Taken together, our findings suggest that the learning-related neural circuits of fast learners are better suited to solving the water maze task than those of slow learners, the latter relying more on structural reorganization to form memory, rather than the relatively economic mechanism of altering synaptic efficacy that is likely used by the former.

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Progressive age‐related development of Alzheimer‐like pathology in APP/PS1 mice

Trinchese

Liu

Battaglia

et al. 2004

Annals of Neurology

327

217

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Increasing evidence points to synaptic plasticity impairment as one of the first events in Alzheimer's disease (AD). However, studies on synaptic dysfunction in different transgenic AD models that overexpress familial AD mutant forms of amyloid precursor protein (APP) and/or presenilin (PS) have provided conflicting results. Both long-term potentiation (LTP) and basal synaptic transmission (BST) have been found to be both unchanged and altered in different models and under differing experimental conditions. Because of their more robust amyloid-beta (Abeta) deposition, double transgenic mice currently are used by several laboratories as an AD model. Here, we report that mice overexpressing APP (K670N:M671L) together with PS1 (M146L) have abnormal LTP as early as 3 months of age. Interestingly, reduced LTP paralleled plaque appearance and increased Abeta levels and abnormal short-term memory (working memory). BST and long-term memory (reference memory) are impaired only later (approximately 6 months) as amyloid burden increases. Abeta pathology across different ages did not correlate with synaptic and cognitive deficits, suggesting that Abeta levels are not a marker of memory decline. In contrast, progression of LTP impairment correlated with the deterioration of working memory, suggesting that percentage of potentiation might be an indicator of the cognitive decline and disease progression in the APP/PS1 mice.

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Strain-dependent Differences in LTP and Hippocampus-dependent Memory in Inbred Mice

Cited by 225 publications

References 48 publications

Hippocampal LTP and memory in mouse strains: Is there evidence for a causal relationship?

Hippocampal LTP and memory in mouse strains: Is there evidence for a causal relationship?

Neurobiological and Endocrine Correlates of Individual Differences in Spatial Learning Ability

Progressive age‐related development of Alzheimer‐like pathology in APP/PS1 mice

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