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Postnatal Migration of Cerebellar Interneurons
Due to its continuing development after birth, the cerebellum represents a unique model for studying the postnatal orchestration of interneuron migration. The combination of fluorescent labeling and ex/in vivo imaging revealed a cellular highway network within cerebellar cortical layers (the externa...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5483635/ https://www.ncbi.nlm.nih.gov/pubmed/28587295 http://dx.doi.org/10.3390/brainsci7060062 |
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author | Galas, Ludovic Bénard, Magalie Lebon, Alexis Komuro, Yutaro Schapman, Damien Vaudry, Hubert Vaudry, David Komuro, Hitoshi |
author_facet | Galas, Ludovic Bénard, Magalie Lebon, Alexis Komuro, Yutaro Schapman, Damien Vaudry, Hubert Vaudry, David Komuro, Hitoshi |
author_sort | Galas, Ludovic |
collection | PubMed |
description | Due to its continuing development after birth, the cerebellum represents a unique model for studying the postnatal orchestration of interneuron migration. The combination of fluorescent labeling and ex/in vivo imaging revealed a cellular highway network within cerebellar cortical layers (the external granular layer, the molecular layer, the Purkinje cell layer, and the internal granular layer). During the first two postnatal weeks, saltatory movements, transient stop phases, cell-cell interaction/contact, and degradation of the extracellular matrix mark out the route of cerebellar interneurons, notably granule cells and basket/stellate cells, to their final location. In addition, cortical-layer specific regulatory factors such as neuropeptides (pituitary adenylate cyclase-activating polypeptide (PACAP), somatostatin) or proteins (tissue-type plasminogen activator (tPA), insulin growth factor-1 (IGF-1)) have been shown to inhibit or stimulate the migratory process of interneurons. These factors show further complexity because somatostatin, PACAP, or tPA have opposite or no effect on interneuron migration depending on which layer or cell type they act upon. External factors originating from environmental conditions (light stimuli, pollutants), nutrients or drug of abuse (alcohol) also alter normal cell migration, leading to cerebellar disorders. |
format | Online Article Text |
id | pubmed-5483635 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-54836352017-06-28 Postnatal Migration of Cerebellar Interneurons Galas, Ludovic Bénard, Magalie Lebon, Alexis Komuro, Yutaro Schapman, Damien Vaudry, Hubert Vaudry, David Komuro, Hitoshi Brain Sci Review Due to its continuing development after birth, the cerebellum represents a unique model for studying the postnatal orchestration of interneuron migration. The combination of fluorescent labeling and ex/in vivo imaging revealed a cellular highway network within cerebellar cortical layers (the external granular layer, the molecular layer, the Purkinje cell layer, and the internal granular layer). During the first two postnatal weeks, saltatory movements, transient stop phases, cell-cell interaction/contact, and degradation of the extracellular matrix mark out the route of cerebellar interneurons, notably granule cells and basket/stellate cells, to their final location. In addition, cortical-layer specific regulatory factors such as neuropeptides (pituitary adenylate cyclase-activating polypeptide (PACAP), somatostatin) or proteins (tissue-type plasminogen activator (tPA), insulin growth factor-1 (IGF-1)) have been shown to inhibit or stimulate the migratory process of interneurons. These factors show further complexity because somatostatin, PACAP, or tPA have opposite or no effect on interneuron migration depending on which layer or cell type they act upon. External factors originating from environmental conditions (light stimuli, pollutants), nutrients or drug of abuse (alcohol) also alter normal cell migration, leading to cerebellar disorders. MDPI 2017-06-06 /pmc/articles/PMC5483635/ /pubmed/28587295 http://dx.doi.org/10.3390/brainsci7060062 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Galas, Ludovic Bénard, Magalie Lebon, Alexis Komuro, Yutaro Schapman, Damien Vaudry, Hubert Vaudry, David Komuro, Hitoshi Postnatal Migration of Cerebellar Interneurons |
title | Postnatal Migration of Cerebellar Interneurons |
title_full | Postnatal Migration of Cerebellar Interneurons |
title_fullStr | Postnatal Migration of Cerebellar Interneurons |
title_full_unstemmed | Postnatal Migration of Cerebellar Interneurons |
title_short | Postnatal Migration of Cerebellar Interneurons |
title_sort | postnatal migration of cerebellar interneurons |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5483635/ https://www.ncbi.nlm.nih.gov/pubmed/28587295 http://dx.doi.org/10.3390/brainsci7060062 |
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