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Article: Secretin Modulates the Postnatal Development of Mouse Cerebellar Cortex Via PKA- and ERK-dependent Pathways

TitleSecretin Modulates the Postnatal Development of Mouse Cerebellar Cortex Via PKA- and ERK-dependent Pathways
Authors
Issue Date2017
PublisherFrontiers Research Foundation. The Journal's web site is located at http://www.frontiersin.org/cellular_neuroscience
Citation
Frontiers in Cellular Neuroscience, 2017, v. 11, p. 382 How to Cite?
AbstractPostnatal development of the cerebellum is critical for its intact function such as motor coordination and has been implicated in the pathogenesis of psychiatric disorders. We previously reported that deprivation of secretin (SCT) from cerebellar Purkinje neurons impaired motor coordination and motor learning function, while leaving the potential role of SCT in cerebellar development to be determined. SCT and its receptor (SCTR) were constitutively expressed in the postnatal cerebellum in a temporal and cell-specific manner. Using a SCT knockout mouse model, we provided direct evidence showing altered developmental patterns of Purkinje cells (PCs) and granular cells (GCs). SCT deprivation reduced the PC density, impaired the PC dendritic formation, induced accelerated GC migration and potentiated cerebellar apoptosis. Furthermore, our results indicated the involvement of protein kinase A (PKA) and extracellular signal regulated kinase (ERK) signaling pathways in SCT-mediated protective effects against neuronal apoptosis. Results of this study illustrated a novel function of SCT in the postnatal development of cerebellum, emphasizing the necessary role of SCT in cerebellar-related functions.
Persistent Identifierhttp://hdl.handle.net/10722/260875
ISSN
2015 Impact Factor: 4.609
2015 SCImago Journal Rankings: 2.219

 

DC FieldValueLanguage
dc.contributor.authorWANG, L-
dc.contributor.authorZhang, L-
dc.contributor.authorChow, BKC-
dc.date.accessioned2018-09-14T08:48:50Z-
dc.date.available2018-09-14T08:48:50Z-
dc.date.issued2017-
dc.identifier.citationFrontiers in Cellular Neuroscience, 2017, v. 11, p. 382-
dc.identifier.issn1662-5102-
dc.identifier.urihttp://hdl.handle.net/10722/260875-
dc.description.abstractPostnatal development of the cerebellum is critical for its intact function such as motor coordination and has been implicated in the pathogenesis of psychiatric disorders. We previously reported that deprivation of secretin (SCT) from cerebellar Purkinje neurons impaired motor coordination and motor learning function, while leaving the potential role of SCT in cerebellar development to be determined. SCT and its receptor (SCTR) were constitutively expressed in the postnatal cerebellum in a temporal and cell-specific manner. Using a SCT knockout mouse model, we provided direct evidence showing altered developmental patterns of Purkinje cells (PCs) and granular cells (GCs). SCT deprivation reduced the PC density, impaired the PC dendritic formation, induced accelerated GC migration and potentiated cerebellar apoptosis. Furthermore, our results indicated the involvement of protein kinase A (PKA) and extracellular signal regulated kinase (ERK) signaling pathways in SCT-mediated protective effects against neuronal apoptosis. Results of this study illustrated a novel function of SCT in the postnatal development of cerebellum, emphasizing the necessary role of SCT in cerebellar-related functions.-
dc.languageeng-
dc.publisherFrontiers Research Foundation. The Journal's web site is located at http://www.frontiersin.org/cellular_neuroscience-
dc.relation.ispartofFrontiers in Cellular Neuroscience-
dc.rightsThis Document is Protected by copyright and was first published by Frontiers. All rights reserved. It is reproduced with permission.-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleSecretin Modulates the Postnatal Development of Mouse Cerebellar Cortex Via PKA- and ERK-dependent Pathways-
dc.typeArticle-
dc.identifier.emailChow, BKC: bkcc@hku.hk-
dc.identifier.authorityChow, BKC=rp00681-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3389/fncel.2017.00382-
dc.identifier.hkuros291535-
dc.identifier.volume11-
dc.identifier.spage382-
dc.identifier.epage382-
dc.publisher.placeSwitzerland-

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