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Neuroinflammation results in dysfunctional mitral cells and olfactory impairment

ABSTRACT: Neuroinflammation results in dysfunctional mitral cells and olfactory impairment

PROVIDER: PRJNA1118241 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29235579_1.fastq.gz	Fastqsanger.gz
	SRR29235579_2.fastq.gz	Fastqsanger.gz
	SRR29235580_1.fastq.gz	Fastqsanger.gz
	SRR29235580_2.fastq.gz	Fastqsanger.gz
	SRR29235581_1.fastq.gz	Fastqsanger.gz

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Neuroinflammation results in dysfunctional mitral cells and olfactory impairment

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Project description:BackgroundOlfactory 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).ResultsReduced olfactory function in EAE was associated with the degeneration of short-axon neurons, immature neurons, and both mitral and tufted cells, along 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 followed by functional validation. Neuroinflammation resulted in the induction of potassium channel transcripts in mitral cells, which was reflected in increased halothane-induced outward currents of these cells, likely contributing to the impaired olfaction in EAE animals.ConclusionThis study reveals the crucial role of mitral cells and their potassium channel activity in the olfactory bulb during EAE, thereby enhancing our understanding of neuroinflammation-induced neurodegeneration in MS.

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