ArticleNeurotoxicity research2016
Caspase-3 is Involved in Aluminum-Induced Impairment of Long-Term Potentiation in Rats Through the Akt/GSK-3β Pathway.
Article in Neurotoxicity research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 40 citations in OpenAlex.
- Brain functional connectivity network alterations in occupational aluminum exposure among workers with mild cognitive impairment.Scientific reports · 2026Article
- Downregulation of Glycogen Synthase Kinase-3 Beta by Urtica dioica L. Contributes to Neuroprotection Against Aluminum Chloride-Mediated Neurotoxicity in Zebrafish Larvae.Molecular neurobiology · 2025Article
- Spirodelae Herba ethanol extract attenuates neurotoxicity in hippocampal cells and improves scopolamine-induced cognitive impairment in mice.Frontiers in pharmacology · 2025Article
- Effects of a Novel Magnesium Complex on Metabolic and Cognitive Functions and the Expression of Synapse-Associated Proteins in Rats Fed a High-Fat Diet.Biological trace element research · 2022Article
- Microencapsulation of Plant Phenolic Extracts Using Complex Coacervation Incorporated in Ultrafiltered Cheese Against AlClFrontiers in nutrition · 2022Article
- The GSK-3β/β-Catenin Signaling-Mediated Brain-Derived Neurotrophic Factor Pathway Is Involved in Aluminum-Induced Impairment of Hippocampal LTP In Vivo.Biological trace element research · 2021Article
- Regulation of mGluR1 on the Expression of PKC and NMDAR in Aluminum-Exposed PC12 Cells.Neurotoxicity research · 2021Article
- Molecular mechanisms of aluminum neurotoxicity: Update on adverse effects and therapeutic strategies.Advances in neurotoxicology · 2021Article
- Effects of Chronic Aluminum Lactate Exposure on Neuronal Apoptosis and Hippocampal Synaptic Plasticity in Rats.Biological trace element research · 2020Article
- Effects of regulating miR-132 mediated GSK-3β on learning and memory function in mice.Experimental and therapeutic medicine · 2020Article
- Aluminum-induced "mixed" cell death in mice cerebral tissue and potential intervention.Neurotoxicity research · 2020Article
- Aluminum-Induced Synaptic Plasticity Impairment via PI3K-Akt-mTOR Signaling Pathway.Neurotoxicity research · 2020Article
- Cognitive impairment of workers in a large-scale aluminium factory in China: a cross-sectional study.BMJ open · 2019Article
- Differential Expression Pattern of Exosome Long Non-Coding RNAs (lncRNAs) and MicroRNAs (miRNAs) in Vascular Endothelial Cells Under Heat Stroke.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Physiological functions of non-apoptotic caspase activity in the nervous system.Seminars in cell & developmental biology · 2018Review
- Article
- Neuroprotective Effects of Higenamine Against the Alzheimer's Disease Via Amelioration of Cognitive Impairment, ADose-response : a publication of International Hormesis SocietyArticle
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A number of studies have indicated that aluminum (Al) exposure can impair learning and memory function. The ability of Al to inhibit hippocampal long-term potentiation (LTP) suggests the possibility of Al impairing synaptic plasticity. LTP is dependent on the externalization of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors (AMPAR). The protein kinase B (Akt) and glycogen synthase kinase-3β (GSK-3β) signaling pathway has been demonstrated to mediate AMPAR delivery. A mechanism by which caspase-3 cleaves Akt is involved in synaptic plasticity, but the underlying molecular mechanism involved has still not been elucidated. The purpose of this study was to investigate the mechanism of LTP impairment and the related signaling pathway disturbance induced by Al exposure. Our results reveal that Al treatment produces a dose-dependent suppression of LTP and decreases in the AMPAR subunits GluR1 and GluR2, in both membrane and total cell extracts. Al caused increased accumulation of active caspase-3 and a gradual decrease in Akt and pGSK-3β. Interestingly, Al depressed LTP and AMPAR protein concentration. N-benzyloxycarbonyl-Asp(OMe)-Glu(OMe)-Val-Asp(OMe)-fluoromethyl ketone (a caspase-3 inhibitor) reversed the Al-induced LTP inhibition, increased levels of active caspase-3, and decreased AMPAR levels in both total and membrane-enriched extracts. It also decreased Akt and pGSK-3β. The molecular mechanism of Al-induced LTP impairment might be related to the activation of caspase-3, cleavage of Akt, activation of GSK-3β, and inhibition of the externalization of AMPAR.
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