2021
DOI: 10.1007/s00213-021-06015-2
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Electroconvulsive seizure inhibits the mTOR signaling pathway via AMPK in the rat frontal cortex

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Cited by 13 publications
(8 citation statements)
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“…We have reported that repeated ECS treatments for 10 days in rats induces autophagy via the activation of AMPK-ULK1-Beclin1 signaling 26 and AMPK-mediated mTOR inhibition 27 in the frontal cortex. AMPK plays a critical role in the autophagy process.…”
Section: Discussionmentioning
confidence: 99%
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“…We have reported that repeated ECS treatments for 10 days in rats induces autophagy via the activation of AMPK-ULK1-Beclin1 signaling 26 and AMPK-mediated mTOR inhibition 27 in the frontal cortex. AMPK plays a critical role in the autophagy process.…”
Section: Discussionmentioning
confidence: 99%
“…26 Our previous study found that the ECS treatments increased the phosphorylation of Raptor, which is another substrate of AMPK and known to suppress mTOR activity, 46 and decreased the phosphorylation of p70S6K and S6, the downstream molecules of mTOR1. 27 To investigate those autophagy-relevant signaling changes by ECS in MPTP PD mouse model, we established our ECS protocol for mouse, 3 times per week for 2 weeks, in a trialand-error manner, but that is very similar to the ECT protocol used in the actual human treatment. In the present study, we observed comparable results with the rat model.…”
Section: Discussionmentioning
confidence: 99%
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“…mTOR can modulate insulin physiology in neurodegenerative studies to increase survival of astrocytes [429], block hyperglycemic endothelial cell injury [430], and preserve metabolic regulation [431]. As a component of the mTOR pathway, the AMP-activated protein kinase (AMPK) modulates cellular metabolism [106,169,198,237,378,381,382,394,432,433], and the activation of AMPK reduces cognitive loss in studies of DM and AD [434,435], removes cerebral Aβ [436] and tau [437], limits Aβ neurotoxicity [392], diminishes long-term inflammation in in the nervous system [10,71,438,439], and fosters pathways for healthy aging [6,440,441].…”
Section: The Mechanistic Target Of Rapamycin and Multiple Sclerosismentioning
confidence: 99%
“…In addition, nicotinamide relies upon AMPK to preserve mitochondria function [261], and Wnt family members employ AMPK to limit neuronal injury [498]. AMPK can maintain electrical activity of the cortex for behavior control [499], AMPK oversees endothelial tight junctions [500], and AMPK can promote mitochondrial integrity during ferroptotic cell death [169]. In the absence of AMPK activity, cell senescence, cell death, and mitochondrial injury can ensue [3,137].…”
Section: Wnt Signaling and Wisp1 Oversight In Diabetes Mellitus And M...mentioning
confidence: 99%