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Deletion of the α subunit of the heterotrimeric Go protein impairs cerebellar cortical development in mice

G(o) is a member of the pertussis toxin-sensitive G(i/o) family. Despite its abundance in the central nervous system, the precise role of G(o) remains largely unknown compared to other G proteins. In the present study, we explored the functions of G(o) in the developing cerebellar cortex by deleting...

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Detalles Bibliográficos
Autores principales: Cha, Hye Lim, Choi, Jung-Mi, Oh, Huy-Hyen, Bashyal, Narayan, Kim, Sung-Soo, Birnbaumer, Lutz, Suh-Kim, Haeyoung
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6585000/
https://www.ncbi.nlm.nih.gov/pubmed/31221179
http://dx.doi.org/10.1186/s13041-019-0477-9
Descripción
Sumario:G(o) is a member of the pertussis toxin-sensitive G(i/o) family. Despite its abundance in the central nervous system, the precise role of G(o) remains largely unknown compared to other G proteins. In the present study, we explored the functions of G(o) in the developing cerebellar cortex by deleting its gene, Gnao. We performed a histological analysis with cerebellar sections of adult mice by cresyl violet- and immunostaining. Global deletion of Gnao induced cerebellar hypoplasia, reduced arborization of Purkinje cell dendrites, and atrophied Purkinje cell dendritic spines and the terminal boutons of climbing fibers from the inferior olivary nucleus. These results indicate that G(o)-mediated signaling pathway regulates maturation of presynaptic parallel fibers from granule cells and climbing fibers during the cerebellar cortical development. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13041-019-0477-9) contains supplementary material, which is available to authorized users.