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Microglial numbers attain adult levels after undergoing a rapid decrease in cell number in the third postnatal week
Open accessAbstract
During postnatal development, microglia, CNS resident innate immune cells, are essential for synaptic pruning, neuronal apoptosis and remodeling. During this period microglia undergo morphological and phenotypic transformations; however, little is known about how microglial number and density is regulated during postnatal CNS development. We found that after an initial increase during the first 14 postnatal days, microglial numbers in mouse brain began declining in the third postnatal week and were reduced by 50% by 6weeks of age; these "adult" levels were maintained until at least 9months of age. Microglial CD11b levels increased, whereas CD45 and ER-MP58 declined between P10 and adulthood, consistent with a maturing microglial phenotype. Our data indicate that both increased microglial apoptosis and a decreased proliferative capacity contribute to the developmental reduction in microglial numbers. We found no correlation between developmental reductions in microglial numbers and brain mRNA levels of Cd200, Cx3Cl1, M-Csf or Il-34. We tested the ability of M-Csf-overexpression, a key growth factor promoting microglial proliferation and survival, to prevent microglial loss in the third postnatal week. Mice overexpressing M-Csf in astrocytes had higher numbers of microglia at all ages tested. However, the developmental decline in microglial numbers still occurred, suggesting that chronically elevated M-CSF is unable to overcome the developmental decrease in microglial numbers. Whereas the identity of the factor(s) regulating microglial number and density during development remains to be determined, it is likely that microglia respond to a "maturation" signal since the reduction in microglial numbers coincides with CNS maturation.
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“Microglia in the first two postnatal weeks are highly proliferative (Nikodemova et al., 2015).”
From Developmental Heterogeneity of Microglia and Brain Myeloid Cells Revealed by Deep Single-Cell RNA Sequencing (2019) · cites this paper as Nikodemova et al., 2015
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Carrier, M., Robert, M.-È., St‐Pierre, M., Ibáñez, F. G., de Andrade, E. G., Savage, J. C., Desjardins, M., & Tremblay, M. (2023) · SSRN Electronic Journal · doi:10.2139/ssrn.4608531
De, I., Maklakova, V. I., Litscher, S. J., Boyd, M. M., Klemm, L. C., Wang, Z., Kendziorski, C. M., & Collier, L. S. (2021) · Figshare · doi:10.6084/m9.figshare.15020525
Smith, A. M., & Grayson, B. E. (2024) · Journal of Neuroscience Research · doi:10.1002/jnr.25364
“Beginning around PND 35, another period of neuronal and microglial apoptosis occurs (Askew & Gomez-Nicola, 2018 ; Majcher-Maślanka et al., 2019 ; Markham et al., 2007 ; Nikodemova et al., 2015; Willing & Juraska, 2015).”
CSF1R-Dependent Microglial Repopulation and Contact-Dependent Inhibition of Proliferation In Vitro
Nakai, R., Kohyama, K., Nishito, Y., & Sakuma, H. (2025) · Brain Sciences · doi:10.3390/brainsci15080825
Stem Cell-Derived 3D Models to Study Alzheimer’s Disease
Inzunza, J., Demetriou, A., Muñoz, P., Arias, J., & Nalvarte, I. (2025) · Stem cell biology and regenerative medicine · doi:10.1007/978-3-031-94101-6_5
Microglial plasticity across development mediates infantile amnesiaPreprint
Stewart, E., Zielke, L. G., Guillaume, G., Boer, A. D., Power, S. D., & Ryan, T. J. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.10.17.683060
De, I., Maklakova, V. I., Litscher, S. J., Boyd, M. M., Klemm, L. C., Wang, Z., Kendziorski, C. M., & Collier, L. S. (2021) · Figshare · doi:10.6084/m9.figshare.15020549
De, I., Maklakova, V. I., Litscher, S. J., Boyd, M. M., Klemm, L. C., Wang, Z., Kendziorski, C. M., & Collier, L. S. (2021) · Figshare · doi:10.6084/m9.figshare.15020540
De, I., Maklakova, V. I., Litscher, S. J., Boyd, M. M., Klemm, L. C., Wang, Z., Kendziorski, C. M., & Collier, L. S. (2021) · Figshare · doi:10.6084/m9.figshare.15020552
De, I., Maklakova, V. I., Litscher, S. J., Boyd, M. M., Klemm, L. C., Wang, Z., Kendziorski, C. M., & Collier, L. S. (2021) · Figshare · doi:10.6084/m9.figshare.15020534
De, I., Maklakova, V. I., Litscher, S. J., Boyd, M. M., Klemm, L. C., Wang, Z., Kendziorski, C. M., & Collier, L. S. (2021) · Figshare · doi:10.6084/m9.figshare.15020546
De, I., Maklakova, V. I., Litscher, S. J., Boyd, M. M., Klemm, L. C., Wang, Z., Kendziorski, C. M., & Collier, L. S. (2021) · Figshare · doi:10.6084/m9.figshare.15020543
De, I., Maklakova, V. I., Litscher, S. J., Boyd, M. M., Klemm, L. C., Wang, Z., Kendziorski, C. M., & Collier, L. S. (2021) · Figshare · doi:10.6084/m9.figshare.15020531
De, I., Maklakova, V. I., Litscher, S. J., Boyd, M. M., Klemm, L. C., Wang, Z., Kendziorski, C. M., & Collier, L. S. (2021) · Figshare · doi:10.6084/m9.figshare.15020528
De, I., Maklakova, V. I., Litscher, S. J., Boyd, M. M., Klemm, L. C., Wang, Z., Kendziorski, C. M., & Collier, L. S. (2021) · Figshare · doi:10.6084/m9.figshare.15020537
Beyeler, S. A., Plunkett, D. L., Watters, J. J., & Huxtable, A. G. (2026) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00669.2025
Mycophenolate mofetil reduces the branching of microglial processes
Teruya, R.-I., Ueda, K., Taketomi, T., Yamamoto, T., Yamashita, N., Konno, H., & Tsuruta, F. (2026) · Molecular Brain · doi:10.1186/s13041-025-01271-1
“To do this, we analyzed the microglial density in vivo by admin-istrating MMF to Cx3cr1 GFP/+ mice from P6 daily and collecting brains at P9 (the midpoint of microglial expansion) and P14 (the general terminal point of microglial expansion) [10, 11] (Fig.”
Inflammatory Mediators Both Directly and Indirectly Promote Microglial Proliferation
Hammond, B. P., Hahn, E., Lee, K. V., Kerr, B. J., & Plemel, J. R. (2026) · Glia · doi:10.1002/glia.70150
“Interleukin-3 is constitutively expressed by subsets of astrocytes throughout the steady state mouse brain (McAlpine et al. 2021), and yet, microglia proliferate minimally in adult-hood (Ginhoux et al. 2010; Kim et al. 2015; Nikodemova et al. 2015).”
In vitro and in vivo study of the effects of Levetiracetam on activated microglia during sepsis
Fleurance, R. (2021) · theses.fr (ABES) · doi:10.70675/0a82ed6ez6595z4366z832fz70cbe839c7ff
Hristovska, I. (2019) · theses.fr (ABES) · doi:10.70675/af1c5105z3e0dz43ffzb906z1553e7a23a6e
Rôle du récepteur 5-HT2B dans la motilité des cellules microgliales
Etienne, F. (2020) · theses.fr (ABES) · doi:10.70675/525a2c9ez9415z45f8z8838z1155f108aaf2
Altérations de la connectivité corticale au cours de périodes critiques du développement
Druart, M. (2020) · theses.fr (ABES) · doi:10.70675/b4f48d73za850z42b2z8dadzfad47d4f0a69
Physiopathologie et modulation de l’activation microgliale secondaire au sepsis
Verdonk, F. (2016) · theses.fr (ABES) · doi:10.70675/8d3a9e0ez15f7z446bzb0e4z56e24e61058a
Mechanisms controlling microglial colonization of the forebrain
Bridlance, C. (2023) · theses.fr (ABES) · doi:10.70675/5879aa36z8649z48f9zb359zf349ce3cb429
MafB and c-Maf transcriptional control of macrophage self-renewal and activation
Huang, H. (2021) · theses.fr (ABES) · doi:10.70675/e3a80f7dz82c4z4f22z8b5eze5bb96e6bf01
Soengkoeng, R., & Clemens, K. J. (2026) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2026.111711
Zhang, X., Gong, M., Chen, Z., Luo, J., Zhao, Z., Wu, Z., Zhao, J., Ma, Y., Nie, L., & Fan, X. (2026) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2026.106794
Osumi, A., Shimamura, T., Miyata, T., & Hattori, Y. (2026) · Neuroscience Research · doi:10.1016/j.neures.2026.105071
Microglial ontogeny and in vitro reconstruction: Bridging development and modeling
Ono, M., Matsuo, H., & Hattori, Y. (2026) · Neuroscience Research · doi:10.1016/j.neures.2026.105078
Chokr, S. M., Jimenez, G., Hoang, J., Mai, D., Liang, H. Y., & Cramer, K. S. (2026) · Hearing Research · doi:10.1016/j.heares.2026.109715
Hove, H. V., Bastos, J., Kancheva, D., Vara‐Pérez, M., Dorion, M., Westermann, F., Ulutekin, C., Shakeri, H., Ali, L., Lievens, A. L., et al. (2026) · Immunity · doi:10.1016/j.immuni.2026.09.002
Metadata
- Authors
- Nikodemova, M., Kimyon, R. S., De, I., Small, A. L., Collier, L. S., & Watters, J. J.
- Affiliations
- University of Wisconsin–Madison (US)
- Corresponding author
- Watters, Jyoti J.
- Venue
- Journal of Neuroimmunology
- Publisher
- Elsevier BV
- Published
- 2015-01
- Volume
- 278
- Pages
- 280-288
- ISSN
- 0165-5728 (ISSN-L)
- PMC
- PMC4297717
- OpenAlex
- W1974031039
- Cited by
- 192
- References
- 56
- Citations by year
- 2026: 16 · 2025: 19 · 2024: 12 · 2023: 20 · 2022: 16 · 2021: 31 · 2020: 24 · 2019: 17 · 2018: 11 · 2017: 11 · 2016: 11 · 2015: 4
- FWCI
- 4.51
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Neuroimmunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (NS049033, HL111598)
- Goldhirsh Foundation
- UW Madison Graduate School
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- microglia, postnatal brain development, microglial apoptosis, microglial proliferation, macrophage colony-stimulating factor, microglial maturation, CD11b, CD45, CD200, fractalkine, IL-34, microglial phenotype
- MeSH terms
- Aging, Animals, Animals, Newborn, Brain, Female, Flow Cytometry, Male, Mice, Inbred ICR, Cytokines, Apoptosis, Microglia, CD11b Antigen, Cell Proliferation, Mice
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