<scp>HFS</scp>‐Triggered <scp>AMPK</scp> Activation Phosphorylates <scp>GSK</scp>3β and Induces E‐<scp>LTP</scp> in Rat Hippocampus <i>In Vivo</i>

Yu, Dan-Fang; Shen, Zu-Cheng; Wu, Pengfei; Guan, Xin-Lei; Chen, Tao; You, Jing; Hu, Zhuang-Li; Ni, Lan; Wang, Fang; Chen, Jianguo; Long, Li‐Hong

doi:10.1111/cns.12532

Cited by 17 publications

(9 citation statements)

References 34 publications

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“…Our data also demonstrate that the energetic metabolic up-regulation mediated by AMPK is crucial for the expression of IEGs, synaptic plasticity and hence memory formation. In line with these results, AMPK was reported to be activated and necessary for LTP induced in vivo by high-frequency stimulation (Yu et al, 2016). However, for a more thorough understanding of these processes, the generation of conditional AMPK knock-out mouse models would help in elucidating the importance of AMPK in cognitive processes.…”

Section: Discussionsupporting

confidence: 58%

AMP-activated protein kinase is essential for the maintenance of energy levels during synaptic activation

Marinangeli

Didier

Ahmed

et al. 2018

Preprint

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While accounting for 2% of the total body mass, the brain is the organ that consumes the most energy. Although it is widely acknowledged that neuronal energy metabolism is tightly regulated, the mechanism how neurons meet their energy demand to sustain synaptic transmission remains poorly studied. Here we provide substantial evidence that the AMP-activated protein kinase (AMPK) plays a leading role in this process. Our results show that following synaptic activation, AMPK activation is required to sustain neuronal energy levels particularly through mitochondrial respiration. Further, our studies revealed that this metabolic plasticity regulated by AMPK is required for the expression of immediate early genes, synaptic plasticity and memory formation. These findings are important in the context of neurodegenerative disorders, as AMPK deregulation as it is observed in Alzheimer’s disease, impairs the metabolic response to synaptic activation. Altogether, our data provides the proof of concept that AMPK is an essential player in the regulation of neuroenergetic metabolism plasticity induced in response to synaptic activation.

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Section: Discussionsupporting

confidence: 58%

AMP-activated protein kinase is essential for the maintenance of energy levels during synaptic activation

Marinangeli

Didier

Ahmed

et al. 2018

Preprint

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“…Western blot was performed as described in our previous studies . After treatment, hippocampal slices were collected and transferred into the Eppendorf tubes, homogenizing with Radio‐Immunoprecipitation Assay (RIPA) buffer (50 mM Tris‐HCl, pH 7.4, 1% NP‐40, 0.5% Na‐deoxycholate, 0.1% Sodium dodecyl sulfate (SDS), 150 mmol/L NaCl, 2 mmol/L EDTA, and 50 mmol/L NaF) including protease and phosphatase inhibitors (10 μL/mg tissue).…”

Section: Methodsmentioning

confidence: 99%

“…Western blot was performed as described in our previous studies. 34 All of the results were presented as a percentage of control following normalization.…”

Section: Western Blotmentioning

confidence: 99%

De‐palmitoylation by N‐(tert‐Butyl) hydroxylamine inhibits AMPAR‐mediated synaptic transmission via affecting receptor distribution in postsynaptic densities

et al. 2018

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“…AMPK is an evolutionarily conserved serine/threonine kinase sensing metabolic changes, including ATP depletion and metabolic stress [25]. Beyond its role in metabolism regulation, accumulating evidence demonstrates that AMPK plays an important role in neural development and neurological function as well as in diseases [59][60][61][62][63]. Previous studies indicate that stress down-regulates AMPK activity and in turn impairs cognitive function [29,64,65].…”

Section: Discussionmentioning

confidence: 99%

Antidiabetic Drug Metformin Ameliorates Depressive-Like Behavior in Mice with Chronic Restraint Stress via Activation of AMP-Activated Protein Kinase

Ai¹,

Fang²,

Hu³

et al. 2020

Aging and disease

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Depression is one of the most prevalent neuropsychiatric disorders in modern society. However, traditional drugs, such as monoaminergic agents, have defect showing lag response requiring several weeks to months. Additionally, these drugs have limited efficacy and high resistance rates in patients with depression. Thus, there is an urgent need to develop novel drugs or approaches for the treatment of depression. Here, using biochemical, pharmacological, genetic and behavioral methods, we demonstrate that metformin imparts a fastacting antidepressant-like effect in naï ve mice as well as stressed mice subjected to chronic restraint stress model. Moreover, inhibition of AMP-activated protein kinase (AMPK) activity by compound C or knock down of hippocampal AMPKα occluded the antidepressant-like effect induced by metformin. Our results suggest that metformin may be a viable therapeutic drug for the treatment of stress-induced depression via activation of AMPK.

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HFS‐Triggered AMPK Activation Phosphorylates GSK3β and Induces E‐LTP in Rat Hippocampus In Vivo

Abstract: Our findings reveal that HFS-triggered AMPK activation phosphorylates GSK3β and induces E-LTP in vivo.

Cited by 17 publications

References 34 publications

AMP-activated protein kinase is essential for the maintenance of energy levels during synaptic activation

AMP-activated protein kinase is essential for the maintenance of energy levels during synaptic activation

De‐palmitoylation by N‐(tert‐Butyl) hydroxylamine inhibits AMPAR‐mediated synaptic transmission via affecting receptor distribution in postsynaptic densities

Antidiabetic Drug Metformin Ameliorates Depressive-Like Behavior in Mice with Chronic Restraint Stress via Activation of AMP-Activated Protein Kinase

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