Olfactory bulb plasticity ensures proper olfaction after severe impairment in postnatal neurogenesis

Abstract The olfactory bulb (OB) neurons establish a complex network that ensures the correct processing of the olfactory inputs. Moreover, the OB presents a lifelong addition of new neurons into its existing circuitry. This neurogenesis is considered essential for the OB function. However, its func...

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Autores principales:	D. Díaz, R. Muñoz-Castañeda, C. Ávila-Zarza, J. Carretero, J. R. Alonso, E. Weruaga
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/212454f65c894d83871020b9a1d32c36
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spelling	oai:doaj.org-article:212454f65c894d83871020b9a1d32c362021-12-02T12:32:50ZOlfactory bulb plasticity ensures proper olfaction after severe impairment in postnatal neurogenesis10.1038/s41598-017-05970-12045-2322https://doaj.org/article/212454f65c894d83871020b9a1d32c362017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-05970-1https://doaj.org/toc/2045-2322Abstract The olfactory bulb (OB) neurons establish a complex network that ensures the correct processing of the olfactory inputs. Moreover, the OB presents a lifelong addition of new neurons into its existing circuitry. This neurogenesis is considered essential for the OB function. However, its functional impact on physiology and behavior is still unclear. Here, we investigate the mechanisms of OB plasticity that underlie bulbar physiology in relation to severe damage of neurogenesis. The neurogenesis of young mice was altered by ionizing radiation. Afterwards, both multi-channel olfactometry and electrophysiological studies were performed. Furthermore, neurogenesis and differentiation of the newly formed cells were assessed using bromodeoxyuridine labeling combined with a wide battery of neuronal markers. Our results demonstrate a reduction in both neurogenesis and volume of the OB in irradiated animals. The number of neuroblasts reaching the OB was reduced and their differentiation rate into interneurons selectively changed; some populations were noticeably affected whereas others remained preserved. Surprisingly, both olfactory detection and discrimination as well as electrophysiology presented almost no alterations in irradiated mice. Our findings suggest that after damaging postnatal neurogenesis, the neurochemical fate of some interneurons changes within a new biological scenario, while maintaining homeostasis and olfaction.D. DíazR. Muñoz-CastañedaC. Ávila-ZarzaJ. CarreteroJ. R. AlonsoE. WeruagaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q D. Díaz R. Muñoz-Castañeda C. Ávila-Zarza J. Carretero J. R. Alonso E. Weruaga Olfactory bulb plasticity ensures proper olfaction after severe impairment in postnatal neurogenesis
description	Abstract The olfactory bulb (OB) neurons establish a complex network that ensures the correct processing of the olfactory inputs. Moreover, the OB presents a lifelong addition of new neurons into its existing circuitry. This neurogenesis is considered essential for the OB function. However, its functional impact on physiology and behavior is still unclear. Here, we investigate the mechanisms of OB plasticity that underlie bulbar physiology in relation to severe damage of neurogenesis. The neurogenesis of young mice was altered by ionizing radiation. Afterwards, both multi-channel olfactometry and electrophysiological studies were performed. Furthermore, neurogenesis and differentiation of the newly formed cells were assessed using bromodeoxyuridine labeling combined with a wide battery of neuronal markers. Our results demonstrate a reduction in both neurogenesis and volume of the OB in irradiated animals. The number of neuroblasts reaching the OB was reduced and their differentiation rate into interneurons selectively changed; some populations were noticeably affected whereas others remained preserved. Surprisingly, both olfactory detection and discrimination as well as electrophysiology presented almost no alterations in irradiated mice. Our findings suggest that after damaging postnatal neurogenesis, the neurochemical fate of some interneurons changes within a new biological scenario, while maintaining homeostasis and olfaction.
format	article
author	D. Díaz R. Muñoz-Castañeda C. Ávila-Zarza J. Carretero J. R. Alonso E. Weruaga
author_facet	D. Díaz R. Muñoz-Castañeda C. Ávila-Zarza J. Carretero J. R. Alonso E. Weruaga
author_sort	D. Díaz
title	Olfactory bulb plasticity ensures proper olfaction after severe impairment in postnatal neurogenesis
title_short	Olfactory bulb plasticity ensures proper olfaction after severe impairment in postnatal neurogenesis
title_full	Olfactory bulb plasticity ensures proper olfaction after severe impairment in postnatal neurogenesis
title_fullStr	Olfactory bulb plasticity ensures proper olfaction after severe impairment in postnatal neurogenesis
title_full_unstemmed	Olfactory bulb plasticity ensures proper olfaction after severe impairment in postnatal neurogenesis
title_sort	olfactory bulb plasticity ensures proper olfaction after severe impairment in postnatal neurogenesis
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/212454f65c894d83871020b9a1d32c36
work_keys_str_mv	AT ddiaz olfactorybulbplasticityensuresproperolfactionaftersevereimpairmentinpostnatalneurogenesis AT rmunozcastaneda olfactorybulbplasticityensuresproperolfactionaftersevereimpairmentinpostnatalneurogenesis AT cavilazarza olfactorybulbplasticityensuresproperolfactionaftersevereimpairmentinpostnatalneurogenesis AT jcarretero olfactorybulbplasticityensuresproperolfactionaftersevereimpairmentinpostnatalneurogenesis AT jralonso olfactorybulbplasticityensuresproperolfactionaftersevereimpairmentinpostnatalneurogenesis AT eweruaga olfactorybulbplasticityensuresproperolfactionaftersevereimpairmentinpostnatalneurogenesis
_version_	1718393905912741888

Olfactory bulb plasticity ensures proper olfaction after severe impairment in postnatal neurogenesis

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