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Secretagogin expression in the mouse olfactory bulb under sensory impairments
The interneurons of the olfactory bulb (OB) are characterized by the expression of different calcium-binding proteins, whose specific functions are not fully understood. This is the case of one of the most recently discovered, the secretagogin (SCGN), which is expressed in interneurons of the glomer...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7726155/ https://www.ncbi.nlm.nih.gov/pubmed/33299042 http://dx.doi.org/10.1038/s41598-020-78499-5 |
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author | Pérez-Revuelta, L. Téllez de Meneses, P. G. López, M. Briñón, J. G. Weruaga, E. Díaz, D. Alonso, J. R. |
author_facet | Pérez-Revuelta, L. Téllez de Meneses, P. G. López, M. Briñón, J. G. Weruaga, E. Díaz, D. Alonso, J. R. |
author_sort | Pérez-Revuelta, L. |
collection | PubMed |
description | The interneurons of the olfactory bulb (OB) are characterized by the expression of different calcium-binding proteins, whose specific functions are not fully understood. This is the case of one of the most recently discovered, the secretagogin (SCGN), which is expressed in interneurons of the glomerular and the granule cell layers, but whose function in the olfactory pathway is still unknown. To address this question, we examined the distribution, generation and activity of SCGN-positive interneurons in the OB of two complementary models of olfactory impairments: Purkinje Cell Degeneration (PCD) and olfactory-deprived mice. Our results showed a significant increase in the density of SCGN-positive cells in the inframitral layers of olfactory-deprived mice as compared to control animals. Moreover, BrdU analyses revealed that these additional SCGN-positive cells are not newly formed. Finally, the neuronal activity, estimated by c-Fos expression, increased in preexisting SCGN-positive interneurons of both deprived and PCD mice -being higher in the later- in comparison with control animals. Altogether, our results suggest that the OB possesses different compensatory mechanisms depending on the type of alteration. Particularly, the SCGN expression is dependent of olfactory stimuli and its function may be related to a compensation against a reduction in sensory inputs. |
format | Online Article Text |
id | pubmed-7726155 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-77261552020-12-14 Secretagogin expression in the mouse olfactory bulb under sensory impairments Pérez-Revuelta, L. Téllez de Meneses, P. G. López, M. Briñón, J. G. Weruaga, E. Díaz, D. Alonso, J. R. Sci Rep Article The interneurons of the olfactory bulb (OB) are characterized by the expression of different calcium-binding proteins, whose specific functions are not fully understood. This is the case of one of the most recently discovered, the secretagogin (SCGN), which is expressed in interneurons of the glomerular and the granule cell layers, but whose function in the olfactory pathway is still unknown. To address this question, we examined the distribution, generation and activity of SCGN-positive interneurons in the OB of two complementary models of olfactory impairments: Purkinje Cell Degeneration (PCD) and olfactory-deprived mice. Our results showed a significant increase in the density of SCGN-positive cells in the inframitral layers of olfactory-deprived mice as compared to control animals. Moreover, BrdU analyses revealed that these additional SCGN-positive cells are not newly formed. Finally, the neuronal activity, estimated by c-Fos expression, increased in preexisting SCGN-positive interneurons of both deprived and PCD mice -being higher in the later- in comparison with control animals. Altogether, our results suggest that the OB possesses different compensatory mechanisms depending on the type of alteration. Particularly, the SCGN expression is dependent of olfactory stimuli and its function may be related to a compensation against a reduction in sensory inputs. Nature Publishing Group UK 2020-12-09 /pmc/articles/PMC7726155/ /pubmed/33299042 http://dx.doi.org/10.1038/s41598-020-78499-5 Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Pérez-Revuelta, L. Téllez de Meneses, P. G. López, M. Briñón, J. G. Weruaga, E. Díaz, D. Alonso, J. R. Secretagogin expression in the mouse olfactory bulb under sensory impairments |
title | Secretagogin expression in the mouse olfactory bulb under sensory impairments |
title_full | Secretagogin expression in the mouse olfactory bulb under sensory impairments |
title_fullStr | Secretagogin expression in the mouse olfactory bulb under sensory impairments |
title_full_unstemmed | Secretagogin expression in the mouse olfactory bulb under sensory impairments |
title_short | Secretagogin expression in the mouse olfactory bulb under sensory impairments |
title_sort | secretagogin expression in the mouse olfactory bulb under sensory impairments |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7726155/ https://www.ncbi.nlm.nih.gov/pubmed/33299042 http://dx.doi.org/10.1038/s41598-020-78499-5 |
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