Genesis of Microglia in the Human Brain

Kershman, John

doi:10.1001/archneurpsyc.1939.02270130034002

Cited by 108 publications

(48 citation statements)

References 15 publications

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“…4B). Such microglial 'hot spots' have been reported in white-matter tracts in rodents (Perry et al 1985;Ashwell, 1991), kittens (Innocenti et al 1983a), and humans (Kershman, 1939;Andjelkovic et al 1998). These microglia clusters, which are transient structures specific to the developing brain, may be 'waiting sites' for glial cells that have entered the brain and will subsequently colonize the parenchyma (del Rio Hortega, 1932;Innocenti et al 1983a).…”

Section: Accumulation Of Intermediate Microglia In Clusters In the Dementioning

confidence: 77%

“…Mononuclear phagocytes penetrate the subpial brain during early embryonic development, before vessel development within the brain parenchyma (Choi, 1981;Cuadros et al 1993;Ling & Wong, 1993;Andjelkovic et al 1998). Several studies have focused on the microglia that are present during various periods of human brain development (Kershman, 1939;Choi, 1981;Fujimoto et al 1989;Esiri et al 1991;Gould & Howard, 1991;Andjelkovic et al 1998;Rezaie & Male, 1999Rezaie, 2003;Rezaie et al 2005;Billiards et al 2006).…”

Section: Introductionmentioning

confidence: 99%

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Early microglial colonization of the human forebrain and possible involvement in periventricular white‐matter injury of preterm infants

et al. 2010

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Amoeboid microglial subpopulations visualized by antibodies against ionized calcium-binding adapter molecule 1, CD68, and CD45 enter the forebrain starting at 4.5 postovulatory or gestational weeks (gw). They penetrate the telencephalon and diencephalon via the meninges, choroid plexus, and ventricular zone. Early colonization by amoeboid microglia-macrophages is first restricted to the white matter, where these cells migrate and accumulate in patches at the junctions of white-matter pathways, such as the three junctions that the internal capsule makes with the thalamocortical projection, external capsule and cerebral peduncle, respectively. In the cerebral cortex anlage, migration is mainly radial and tangential towards the immature white matter, subplate layer, and cortical plate, whereas pial cells populate the prospective layer I. A second wave of microglial cells penetrates the brain via the vascular route at about 12-13 gw and remains confined to the white matter. Two main findings deserve emphasis. First, microglia accumulate at 10-12 gw at the cortical plate-subplate junction, where the first synapses are detected. Second, microglia accumulate in restricted laminar bands, most notably around 19-30 gw, at the axonal crossroads in the white matter (semiovale centre) rostrally, extending caudally in the immature white matter to the visual radiations. This accumulation of proliferating microglia is located at the site of white-matter injury in premature neonates. The spatiotemporal organization of microglia in the immature white and grey matter suggests that these cells may play active roles in developmental processes such as axonal guidance, synaptogenesis, and neurodevelopmental apoptosis as well as in injuries to the developing brain, in particular in the periventricular white-matter injury of preterm infants.

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Section: Accumulation Of Intermediate Microglia In Clusters In the Dementioning

confidence: 77%

Section: Introductionmentioning

confidence: 99%

Early microglial colonization of the human forebrain and possible involvement in periventricular white‐matter injury of preterm infants

et al. 2010

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“…Following the initial observational studies carried out in man [28][29][30], work on the origin of microglia was continued principally in rodents [31][32][33][34][35][36][37][38][39][40]. A view has now emerged that essentially assigns the origin of these cells as bloodderived mononuclear phagocytes, whose phenotype is determined by the CNS microenvironment [27].…”

Section: Colonisation Of the Cns By Microgliamentioning

confidence: 99%

“…The original studies of von Sá ntha and Juba [30] and Kershman [29] had shown that microglial cells could be identified in the human CNS from as early as 10 weeks of gestation. Although occasional mononuclear phagocytes have been identified in the CNS at very early stages of gestation, even before vascularisation [55,56], these tend to be isolated cells, and the main phase of colonisation occurs within the second trimester of development in the telencephalon and a few weeks earlier in the spinal cord [56,57].…”

Section: Timing and Location Of Colonisation In Manmentioning

confidence: 99%

“…Although occasional mononuclear phagocytes have been identified in the CNS at very early stages of gestation, even before vascularisation [55,56], these tend to be isolated cells, and the main phase of colonisation occurs within the second trimester of development in the telencephalon and a few weeks earlier in the spinal cord [56,57]. In man and a variety of other species, including cat, dog, and rat, the timing of the major influx of microglia appears to correlate with vascularisation of the CNS [28][29][30]. At birth, microglia are extensively distributed throughout all areas of the brain by which time they have started to develop the characteristic distribution and the ramified phenotype seen in resting adult microglia (reviewed in Rezaie and Male [5]).…”

Section: Timing and Location Of Colonisation In Manmentioning

confidence: 99%

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Differentiation, Ramification and Distribution of Microglia within the Central Nervous System Examined

Rezaie

Male

2001

Neuroembryol Aging

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The central nervous system contains several populations of mononuclear phagocytes. Principal amongst these are the tissue-resident microglia. These cells are considered to derive from circulating blood progenitors that colonise the developing human nervous system in the second trimester of fetal life. They first appear as amoeboid forms and gradually differentiate to process-bearing ‘ramified’ forms with maturation. Signals driving this transformation are known to be partly derived from astrocytes in vitro, and amoeboid microglial cells progressively ramify when co-cultured with astrocytes, mirroring the ‘differentiation’ of microglia in situ during development. In the adult, microglia occupy distinct non-overlapping territories in their ramified conformations, and are capable of ‘dedifferentiating’ to their activated amoeboid morphological states in a number of pathological circumstances. This is in keeping with the capacity of these cells for a rapid response to inflammatory cues in the CNS. The interchangeable morphological continuum of these cells supports the view that microglia represent a single heterogeneous population of resident mononuclear phagocytes capable of marked plasticity. This review will discuss signals that drive the colonisation, differentiation and ramification of microglia, and examines hypothetical models for their spatial distribution in the adult nervous system.

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Colonisation of the developing human brain and spinal cord by microglia: a review

Rezaie¹,

Male²

1999

Microsc. Res. Tech.

177

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Genesis of Microglia in the Human Brain

Cited by 108 publications

References 15 publications

Early microglial colonization of the human forebrain and possible involvement in periventricular white‐matter injury of preterm infants

Early microglial colonization of the human forebrain and possible involvement in periventricular white‐matter injury of preterm infants

Differentiation, Ramification and Distribution of Microglia within the Central Nervous System Examined

Colonisation of the developing human brain and spinal cord by microglia: a review

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