Absence of colony stimulation factor-1 receptor results in loss of microglia, disrupted brain development and olfactory deficits.

The brain contains numerous mononuclear phagocytes called microglia. These cells express the transmembrane tyrosine kinase receptor for the macrophage growth factor colony stimulating factor-1 (CSF-1R). Using a CSF-1R-GFP reporter mouse strain combined with lineage defining antibody staining we show...

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Autores principales:	Bryna Erblich, Liyin Zhu, Anne M Etgen, Kostantin Dobrenis, Jeffrey W Pollard
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/8cee0425a3a34507824107fea8245bce
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spelling	oai:doaj.org-article:8cee0425a3a34507824107fea8245bce2021-11-18T07:35:37ZAbsence of colony stimulation factor-1 receptor results in loss of microglia, disrupted brain development and olfactory deficits.1932-620310.1371/journal.pone.0026317https://doaj.org/article/8cee0425a3a34507824107fea8245bce2011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22046273/?tool=EBIhttps://doaj.org/toc/1932-6203The brain contains numerous mononuclear phagocytes called microglia. These cells express the transmembrane tyrosine kinase receptor for the macrophage growth factor colony stimulating factor-1 (CSF-1R). Using a CSF-1R-GFP reporter mouse strain combined with lineage defining antibody staining we show in the postnatal mouse brain that CSF-1R is expressed only in microglia and not neurons, astrocytes or glial cells. To study CSF-1R function we used mice homozygous for a null mutation in the Csflr gene. In these mice microglia are >99% depleted at embryonic day 16 and day 1 post-partum brain. At three weeks of age this microglial depletion continues in most regions of the brain although some contain clusters of rounded microglia. Despite the loss of microglia, embryonic brain development appears normal but during the post-natal period the brain architecture becomes perturbed with enlarged ventricles and regionally compressed parenchyma, phenotypes most prominent in the olfactory bulb and cortex. In the cortex there is increased neuronal density, elevated numbers of astrocytes but reduced numbers of oligodendrocytes. Csf1r nulls rarely survive to adulthood and therefore to study the role of CSF-1R in olfaction we used the viable null mutants in the Csf1 (Csf1(op)) gene that encodes one of the two known CSF-1R ligands. Food-finding experiments indicate that olfactory capacity is significantly impaired in the absence of CSF-1. CSF-1R is therefore required for the development of microglia, for a fully functional olfactory system and the maintenance of normal brain structure.Bryna ErblichLiyin ZhuAnne M EtgenKostantin DobrenisJeffrey W PollardPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 10, p e26317 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Bryna Erblich Liyin Zhu Anne M Etgen Kostantin Dobrenis Jeffrey W Pollard Absence of colony stimulation factor-1 receptor results in loss of microglia, disrupted brain development and olfactory deficits.
description	The brain contains numerous mononuclear phagocytes called microglia. These cells express the transmembrane tyrosine kinase receptor for the macrophage growth factor colony stimulating factor-1 (CSF-1R). Using a CSF-1R-GFP reporter mouse strain combined with lineage defining antibody staining we show in the postnatal mouse brain that CSF-1R is expressed only in microglia and not neurons, astrocytes or glial cells. To study CSF-1R function we used mice homozygous for a null mutation in the Csflr gene. In these mice microglia are >99% depleted at embryonic day 16 and day 1 post-partum brain. At three weeks of age this microglial depletion continues in most regions of the brain although some contain clusters of rounded microglia. Despite the loss of microglia, embryonic brain development appears normal but during the post-natal period the brain architecture becomes perturbed with enlarged ventricles and regionally compressed parenchyma, phenotypes most prominent in the olfactory bulb and cortex. In the cortex there is increased neuronal density, elevated numbers of astrocytes but reduced numbers of oligodendrocytes. Csf1r nulls rarely survive to adulthood and therefore to study the role of CSF-1R in olfaction we used the viable null mutants in the Csf1 (Csf1(op)) gene that encodes one of the two known CSF-1R ligands. Food-finding experiments indicate that olfactory capacity is significantly impaired in the absence of CSF-1. CSF-1R is therefore required for the development of microglia, for a fully functional olfactory system and the maintenance of normal brain structure.
format	article
author	Bryna Erblich Liyin Zhu Anne M Etgen Kostantin Dobrenis Jeffrey W Pollard
author_facet	Bryna Erblich Liyin Zhu Anne M Etgen Kostantin Dobrenis Jeffrey W Pollard
author_sort	Bryna Erblich
title	Absence of colony stimulation factor-1 receptor results in loss of microglia, disrupted brain development and olfactory deficits.
title_short	Absence of colony stimulation factor-1 receptor results in loss of microglia, disrupted brain development and olfactory deficits.
title_full	Absence of colony stimulation factor-1 receptor results in loss of microglia, disrupted brain development and olfactory deficits.
title_fullStr	Absence of colony stimulation factor-1 receptor results in loss of microglia, disrupted brain development and olfactory deficits.
title_full_unstemmed	Absence of colony stimulation factor-1 receptor results in loss of microglia, disrupted brain development and olfactory deficits.
title_sort	absence of colony stimulation factor-1 receptor results in loss of microglia, disrupted brain development and olfactory deficits.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/8cee0425a3a34507824107fea8245bce
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Absence of colony stimulation factor-1 receptor results in loss of microglia, disrupted brain development and olfactory deficits.

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