Multiple cellular cascades participate in long-term potentiation and in hippocampus-dependent learning

Baudry, Michel; Zhu, Guoqi; Liu, Yan; Wang, Yubin; Briz, Victor; Bi, Xiaoning

doi:10.1016/j.brainres.2014.11.033

Cited by 89 publications

(44 citation statements)

References 73 publications

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“…Thus the same biochemical machinery providing a molecular brake on LTP is involved in limiting the extent of learning of hippocampus-dependent tasks. We previously argued that such a mechanism could account for the beneficial effects of space training as opposed to massed training (Baudry et al, 2014; Shimizu et al, 2007; Wang et al, 2013). …”

Section: Discussionmentioning

confidence: 99%

A calpain-2 selective inhibitor enhances learning & memory by prolonging ERK activation

et al. 2016

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While calpain-1 activation is required for LTP induction by theta burst stimulation (TBS), calpain-2 activation limits its magnitude during the consolidation period. A selective calpain-2 inhibitor applied either before or shortly after TBS enhanced the degree of potentiation. In the present study, we tested whether the selective calpain-2 inhibitor, Z-Leu-Abu-CONH-CH2-C6H3 (3, 5-(OMe)2 (C2I), could enhance learning and memory in wild-type (WT) and calpain-1 knockout (C1KO) mice. We first showed that C2I could reestablish TBS-LTP in hippocampal slices from C1KO mice, and this effect was blocked by PD98059, an inhibitor of ERK. TBS resulted in PTEN degradation in hippocampal slices from both WT and C1KO mice, and C2I treatment blocked this effect in both mouse genotypes. Systemic injection of C2I 30 min before training in the fear-conditioning paradigm resulted in a biphasic dose-response curve, with low doses enhancing and high doses inhibiting freezing behavior. The difference between the doses needed to enhance and inhibit learning matches the difference in concentrations producing inhibition of calpain-2 and calpain-1. A low dose of C2I also restored normal learning in a novel object recognition task in C1KO mice. Levels of SCOP, a ERK phosphatase known to be cleaved by calpain-1, were decreased in dorsal hippocampus early but not late following training in WT mice; C2I treatment did not affect the early decrease in SCOP levels but prevented its recovery at the later time-point and prolonged ERK activation. The results indicate that calpain-2 activation limits the extent of learning, an effect possibly due to temporal limitation of ERK activation, as a result of SCOP synthesis induced by calpain-2-mediated PTEN degradation.

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Section: Discussionmentioning

confidence: 99%

A calpain-2 selective inhibitor enhances learning & memory by prolonging ERK activation

et al. 2016

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“…Ca 2+ influx has important implications for long‐term changes in synaptic efficacy as it triggers cascades of second‐messenger systems within the cell. This can lead to LTP or long‐term depression (LTD; a decrease in synaptic efficacy), depending on whether the change in intracellular Ca 2+ concentration is large or small (Baudry et al., ; Cormier, Greenwood, & Connor, ).…”

Section: Ltp Effects Evoked By Electrical Stimulation In Vitro and Inmentioning

confidence: 99%

A review of plasticity induced by auditory and visual tetanic stimulation in humans

Sanders

Thompson

Corballis

et al. 2018

Eur J of Neuroscience

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Long-term potentiation is a form of synaptic plasticity thought to play an important role in learning and memory. Recently noninvasive methods have been developed to induce and measure activity similar to long-term potentiation in humans. Sensory tetani (trains of quickly repeating auditory or visual stimuli) alter the electroencephalogram in a manner similar to electrical stimulation that results in long-term potentiation. This review briefly covers the development of long-term potentiation research before focusing on in vivo human studies that produce long-term potentiation-like effects using auditory and visual stimulation. Similarities and differences between traditional (animal and brain tissue) long-term potentiation studies and human sensory tetanization studies will be discussed, as well as implications for perceptual learning. Although evidence for functional consequences of sensory tetanization remains scarce, studies involving clinical populations indicate that sensory induced plasticity paradigms may be developed into diagnostic and research tools in clinical settings. Individual differences in the effects of sensory tetanization are not well-understood and provide an interesting avenue for future research. Differences in effects found between research groups that have emerged as the field has progressed are also yet to be resolved.

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“…As an important electrophysiological mechanism of learning and memory, LTP is a long-lasting increase in synaptic efficacy which follows high-frequency stimulation of afferent fibers (49). Our previous study showed that Aβ1-40-induced damage of late phase LTP, learning and memory were antagonized by Val 8 -GLP-1 (10).…”

Section: Discussionmentioning

confidence: 99%

Exendin-4 antagonizes Aβ1-42-induced attenuation of spatial learning and memory ability

Wang¹,

Wang²,

Jiang³

et al. 2016

Experimental and Therapeutic Medicine

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β-amyloid protein (Aβ) accumulation in cerebral centers involved in cognition and memory is a pivotal pathological feature of Alzheimer's disease (AD). The onset process of type 2 diabetes mellitus (T2DM) has a number of similarities compared with AD. Thus, it is hypothesized that the pharmacological therapy employed for the treatment of T2DM may help to prevent and ameliorate the symptoms of AD. This study demonstrated that Exendin-4, which is a glucagon-like peptide-1 analogue which is used as a therapeutic drug for T2DM, markedly antagonized Aβ fragment-induced attenuation of spatial learning and memory ability, as indicated by a Morris water maze experiment. In addition, we investigated the potential underlying electrophysiological and molecular mechanisms. The results indicate that Exendin-4 rescued long-term potentiation from Aβ1-42-induced damage in the rat hippocampal CA1 region in vivo, and antagonized Aβ1-42-induced reduction of cyclic adenosine monophosphate and phosphorylated-cAMP response element-binding protein in rat hippocampal tissue using ELISA and western blot analysis, respectively. Thus, the results of the present study provide theoretical support for the application of Exendin-4 for improving AD.

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Multiple cellular cascades participate in long-term potentiation and in hippocampus-dependent learning

Cited by 89 publications

References 73 publications

A calpain-2 selective inhibitor enhances learning & memory by prolonging ERK activation

A calpain-2 selective inhibitor enhances learning & memory by prolonging ERK activation

A review of plasticity induced by auditory and visual tetanic stimulation in humans

Exendin-4 antagonizes Aβ1-42-induced attenuation of spatial learning and memory ability

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