ArticleNeurochemical research2025
Frequency-Dependent Mechanism of 24-Hydroxycholesterol-Mediated Modulation of Neurotransmitter Release at the Mouse Neuromuscular Junction: The Role of Reactive Oxygen Species.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Acute mitochondrial dysfunction impairs neuromuscular transmission and contractility in mouse diaphragm: the protective potential of 25-hydroxycholesterol.Journal of physiology and biochemistry · 2026Article
- Nanomolar Cadmium Disrupts Neurotransmitter Release Timing via a ROS-dependent Mechanism at the Mouse Neuromuscular Junction: Modulation by Nanomolar ZnNeurochemical research · 2026Article
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Authors and funding
3 authors.
Funding
Abstract
Neuron-specific enzyme CYP46A1 converts cholesterol to 24-hydroxycholesterol (24-HC), which crosses the brain blood barrier, entering the systemic circulation. Production of 24-HC depends on synaptic and metabolic activity and changes significantly during aging and neurodegenerative diseases. Previously, it was shown that prolonged application of 24-HC (0.4 µM) suppressed recruitment of synaptic vesicles to exocytosis during 20 Hz nerve stimulation acting via elevation of NO synthesis at the mouse neuromuscular junctions (NMJs). Here, using microelectrode recording of postsynaptic responses and fluorescent trackers for endo-exocytosis, NO and reactive oxygen species (ROS) production, the effect of 24-HC on neuromuscular transmission at 10 Hz and 70 Hz nerve firing was studied. At 10 Hz stimulation, 24-HC decreased neurotransmitter release and synaptic vesicle involvement in exocytosis. This was associated with elevation of NO synthesis without marked changes in ROS generation. However, at 70 Hz activity, 24-HC increased the recruitment of synaptic vesicles in exocytosis in combination with attenuation of NO synthesis and enhancement of ROS production. 24-HC-mediated increase in ROS production was suppressed by NADPH-oxidase inhibitor VAS2870, and antioxidant N-acetylcysteine completely prevented 24-HC-dependent potentiation of neurotransmission and suppression of NO synthesis during 70 Hz activity. Similarly, protein kinase C inhibitor chelerythrine blocked 24-HC-mediated enhancement of exocytosis and attenuation of NO generation at 70 Hz stimulation. Thus, 24-HC suppresses neurotransmission at moderate-frequency activity, probably via elevation of NO synthesis, but it potentiates neurotransmitter release and synaptic vesicle recruitment into exocytosis during high-frequency nerve firing via an NADPH oxidase/ROS/protein kinase C pathway.
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