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Neuroinflammation results in dysfunctional mitral cells and olfactory impairment

GSE268675 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2024/12/31 Platform GPL24247
Summary
Olfactory dysfunction is an underestimated symptom in multiple sclerosis (MS). Here, we examined the pathogenic mechanisms underlying inflammation-induced dysfunction of the olfactory bulb using the animal model of MS, experimental autoimmune encephalomyelitis (EAE). Reduced olfactory function in EAE was associated with the degeneration of short-axon neurons, immature neurons, and mitral cells, together with their synaptic interactions and axonal repertoire. To dissect the mechanisms underlying the susceptibility of mitral cells, the main projection neurons of the olfactory bulb, we profiled their responses to neuroinflammation by single-nucleus RNA sequencing. Neuroinflammation resulted in the induction of potassium channel transcripts in mitral cells, which was reflected in reduced halothane-induced outward currents of these cells, likely contributing to the impaired olfaction in EAE animals.
Published in
Neuroinflammation causes mitral cell dysfunction and olfactory impairment in a multiple sclerosis model
Schubert C, Schulz K, Sonner JK et al. · Journal of neuroinflammation 2025 · PMID 40057769 · doi:10.1186/s12974-025-03388-5
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Also filed as BioProject PRJNA1118241 and SRA study SRP510840. Searching any of these in the dataset finder brings you back here.

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