Commissural and monosynaptic inputs to medial vestibular nucleus GABAergic neurons in mice.

GABAergic neurons medial vestibular nucleus vestibular compensation vestibular disorders vestibular function

Journal

Frontiers in neurology
ISSN: 1664-2295
Titre abrégé: Front Neurol
Pays: Switzerland
ID NLM: 101546899

Informations de publication

Date de publication:
2024
Historique:
received: 21 08 2024
accepted: 18 09 2024
medline: 23 10 2024
pubmed: 23 10 2024
entrez: 23 10 2024
Statut: epublish

Résumé

MVN GABAergic neurons is involved in the rebalance of commissural system contributing to alleviating acute peripheral vestibular dysfunction syndrome. This study aims to depict monosynaptic inputs to MVN GABAergic neurons. The modified rabies virus-based retrogradation method combined with the VGAT-IRES-Cre mice was used in this study. Moreover, the commissural connections with MVN GABAergic neurons were analyzed. We identified 60 nuclei projecting to MVN GABAergic neurons primarily distributed in the cerebellum and the medulla. The uvula-nodulus, gigantocellular reticular nucleus, prepositus nucleus, intermediate reticular nucleus, and three other nuclei sent dense inputs to MVN GABAergic neurons. The medial (fastigial) cerebellar nucleus, dorsal paragigantocellular nucleus, lateral paragigantocellular nucleus and 10 other nuclei sent moderate inputs to MVN GABAergic neurons. Sparse inputs to MVN GABAergic neurons originated from the nucleus of the solitary tract, lateral reticular nucleus, pedunculopontine tegmental nucleus and 37 other nuclei. The MVN GABAergic neurons were regulated by the contralateral MVN, lateral vestibular nucleus, superior vestibular nucleus, and inferior vestibular nucleus. Our study contributes to further understanding of the vestibular dysfunction in terms of neural circuits and search for new strategies to facilitate vestibular compensation.

Identifiants

pubmed: 39440253
doi: 10.3389/fneur.2024.1484488
pmc: PMC11493639
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1484488

Informations de copyright

Copyright © 2024 Kong, Kong, Liu, Wu, Wang and Dai.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Auteurs

Dedi Kong (D)

Department of Otology and Skull Base Surgery, Eye Ear Nose and Throat Hospital, Fudan University, Shanghai, China.
Key Laboratory of Hearing Medicine, Ministry of Health, Eye Ear Nose and Throat Hospital, Fudan University, Shanghai, China.

Lingxi Kong (L)

Department of Pharmacology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, and Institutes of Brain Science, Fudan University, Shanghai, China.

Chengwei Liu (C)

Department of Otology and Skull Base Surgery, Eye Ear Nose and Throat Hospital, Fudan University, Shanghai, China.
Key Laboratory of Hearing Medicine, Ministry of Health, Eye Ear Nose and Throat Hospital, Fudan University, Shanghai, China.

Qianru Wu (Q)

Department of Otology and Skull Base Surgery, Eye Ear Nose and Throat Hospital, Fudan University, Shanghai, China.
Key Laboratory of Hearing Medicine, Ministry of Health, Eye Ear Nose and Throat Hospital, Fudan University, Shanghai, China.

Jing Wang (J)

Department of Otology and Skull Base Surgery, Eye Ear Nose and Throat Hospital, Fudan University, Shanghai, China.
Key Laboratory of Hearing Medicine, Ministry of Health, Eye Ear Nose and Throat Hospital, Fudan University, Shanghai, China.

Chunfu Dai (C)

Department of Otology and Skull Base Surgery, Eye Ear Nose and Throat Hospital, Fudan University, Shanghai, China.
Key Laboratory of Hearing Medicine, Ministry of Health, Eye Ear Nose and Throat Hospital, Fudan University, Shanghai, China.

Classifications MeSH