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Dysregulated autophagy, neural signaling pathways and gut-brain axis in a novel vestibular migraine-like rat model: implications for pathogenesis
Disrupted cellular cleanup, brain nerve signals, and gut-brain communication in a new rat model of vestibular migraine: possible causes
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Abstract
-like rats exhibited significant mechanical and thermal hyperalgesia, with p < 0.05.
- Mechanical and thermal hyperalgesia was observed in VM-like rats, along with longer balance beam traversal and higher motion sickness index scores.
- Molecular analysis indicated upregulation of pain-related channels (TRPA1, TRPV1, TRPM8) in blood and increased CGRP levels in specific brain regions.
- Activation of the NMDAR1-CaMKII-CREB signaling pathway was noted in the vestibular nuclei of VM-like rats.
- Impaired autophagic processes were identified in both VM patients and VM-like rats, evidenced by elevated levels of LC3-II and P62.
- Alterations in gut microbiota included reduced diversity and changes in specific bacterial populations, such as increased Lactobacillus and decreased Lachnospiraceae.
- Serum metabolomics showed a decrease in certain phospholipids and an increase in metabolites like 2-ketobutyric acid and GABA, indicating shifts in metabolic pathways.
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Key numbers
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Increase in Levels
levels were significantly increased in and of rats.
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Mechanical Hyperalgesia
rats exhibited significant mechanical hyperalgesia compared to group.
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Elevated Motion Sickness Index
rats showed significantly elevated index scores from day 3 onwards.