ArticleBrain research2025
Acute high glucose exposure impairs synaptosomal vesicle release activity.
Article in Brain research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Lysosomal dysfunction in diabetes and diabetic complications.Frontiers in endocrinology · 2026Review
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3 authors.
Funding
Abstract
backgroundIncreasing evidence indicates an association between Alzheimer's disease (AD) and diabetes. AD and diabetic brains share a hyperglycemic phenotype, making it a plausible mechanistic link between the two diseases. The vacuolar-type ATPase (V-ATPase) is essential for neurotransmitter concentration in synaptic vesicles and subsequent neuronal transmission. However, its role in AD pathogenesis is unclear.
objectivesWe sought to examine whether acute hyperglycemic exposure would alter synaptic vesicular exocytosis and V-ATPase function in synaptosomes freshly extracted from wildtype mouse brains.
methodsSynaptic exocytosis was studied by analyzing the synaptosomal release of the fluorescent dye acridine orange (AO) and the neurotransmitter glutamate. Synaptic V-ATPase activity was assessed by measuring V-ATPase assembly using co-immunoprecipitation and V-ATPase-released phosphates.
resultsAcute hyperglycemia reduced synaptic vesicular exocytosis as indicated by attenuated AO and glutamate release. Moreover, acute hyperglycemia reduced synaptic V-ATPase assembly but not V-ATPase-released phosphates.
conclusionsThe present work demonstrates that hyperglycemia can impair synaptic vesicular exocytosis, partially by reducing V-ATPase assembly. We hypothesize that these molecular changes can be a shared mechanistic contributor to synaptic dysfunction in AD and diabetes. Further studies are needed to investigate the impact of chronic hyperglycemia and glycolytic metabolism on synaptic vesicular activity and V-ATPase function in animal models of AD and diabetes.
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