Amoeboid and ramified microglia: Their interrelationship and response to brain injury

Leong, Siew Meng; Ling, Eng‐Ang

doi:10.1002/glia.440060106

Cited by 117 publications

(83 citation statements)

References 27 publications

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“…6). These events were described by del Rio-Hortega (1932), and received later support from morphological observations of intermediate forms between ameboid and rami®ed microglial cells (Ling, 1981;Perry et al, 1985;Leong and Ling, 1992;Wu et al, 1992Wu et al, , 1993Cuadros et al, 1994). The transformation of ameboid microglia into rami®ed microglia is now largely accepted (Perry and Gordon, 1988;Ling and Wong, 1993;Davis et al, 1994;Barron, 1995).…”

Section: Differentiation Of Microglial Cellsmentioning

confidence: 85%

The origin and differentiation of microglial cells during development

Cuadros

Navascués

1998

Progress in Neurobiology

269

177

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AbstractÐSome authors claim that microglia originate from the neuroepithelium, although most now believe that microglial cells are of mesodermal origin, and probably belong to the monocyte/macrophage cell line. These cells must enter the developing central nervous system (CNS) from the blood stream, the ventricular space or the meninges. Afterward microglial cells are distributed more or less homogeneously through the entire nervous parenchyma. Stereotyped patterns of migration have been recognized during development, in which long-distance tangential migration precedes radial migration of individual cells. Microglial cells moving through the nervous parenchyma are ameboid microglia, which apparently di erentiate into rami®ed microglia after reaching their de®nitive location. This is supported by the presence of cells showing intermediate features between those of ameboid and rami®ed microglia. The factors that control the invasion of the nervous parenchyma, migration within the developing CNS and di erentiation of microglial cells are not well known. These phenomena apparently depend on environmental factors such as soluble or cell-surface bound molecules and components of the extracellular matrix. Microglial cells within the developing CNS are involved in clearing cell debris and withdrawing misdirected or transitory axons, and presumably support cell survival and neurite growth. #

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Section: Differentiation Of Microglial Cellsmentioning

confidence: 85%

The origin and differentiation of microglial cells during development

Cuadros

Navascués

1998

Progress in Neurobiology

269

177

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“…These cells, which exhibit features indicative of phagocytosis and which share common characteristics with their monocytic precursors (Yee et al, 1990;Ling et al, 19921, would seem likely candidates to become activated and proliferate after injury. However, recent work showed that ameboid cells do not migrate to the site of a stab wound cortical injury in the newborn brain (Leong and Ling, 1992) and that the major cell type responding to neonatal brain injury is the bloodborne phagocyte (Milligan et al, 1991). These findings, together with previous studies showing vascular sprouting in the middle layers of the 7-day-old rat neocortex (Hurley and Streit, 1991), the immaturity of the rat blood-brain barrier until 12 days after birth (Xu et al, 19931, and a blood-brain barrier disruption during the first 24 hours following the injection of an excitotoxin (Andersson et al, 1991a), support the possibility that most of the increase in tomato lectin-positive cells, seen at 3 days after the lesion, is due to a peripheral monocytic recruitment.…”

Section: Pattern Of Microglial Responsementioning

confidence: 98%

Microglial response to N-methyl-D-aspartate-mediated excitotoxicity in the immature rat brain

et al. 1996

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The intracerebral injection of N-methyl-D-aspartate (NMDA) has been proposed as a model for hypoxic-ischemic insult in the immature brain. In this light, the aim of this study was to describe the time course of the microglial reaction in the areas undergoing primary degeneration at the site of intracortical NMDA injection as well as in areas undergoing secondary anterograde and/or retrograde degeneration. Fifty nanomoles of NMDA were injected in the sensorimotor cortex of 6-day-old rats. After survival times ranging from 10 hours to 28 days, cryostat sections were stained for routine histology and for the demonstration of microglial cells by means of tomato lectin histochemistry. The areas affected by primary degeneration caused by the intracortical injection of NMDA were the neocortex, the hippocampus, and the rostral thalamus. Secondary degeneration (retrograde and anterograde) was observed in the ventrobasal complex of the thalamus. The cortical lesion also caused Wallerian degeneration of the cortical descending efferents as observed in the basilar pons. Microglial reactivity in all these areas was present at 10 hours postinjection and was restricted to the areas undergoing neuronal or axonal degeneration. Reactive microglial cells were stained intensely and showed a round or pseudopodic morphology. At 3 days, an apparent increase in the number of tomato lectin-positive cells was observed in the areas undergoing neuronal death. By 7 days after the injection, the lesion became nonprogressive, and by 14 and 28 days, microglial cells showed moderate lectin binding and a more ramified morphology.

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“…Third, there are the amoeboid microglial cells, known also as ''gitter'' or ''reactive'' microglia. These amoeboid cells have been described in the cerebral white matter, particularly in the corpus callosum, of the developing brain (Ling, 1976;Imamoto and Leblond, 1978;Valentino and Jones, 1981;Innocenti et al, 1983a,b;Leong et al, 1983;Lent et al, 1985;Boya et al, 1991;Chugani et al, 1991;Ling et al, 1991;Milligan et al, 1991a,b;Leong and Ling, 1992). These cells are of blood monocyte lineage and immigrate into the white matter from the vascular system during late embryonic and early postnatal life (Imamoto and Leblond, 1978;Ling et al, 1980Ling et al, , 1982Perry et al, 1985;Perry and Gordon, 1988;Boya et al, 1991;Chugani et al, 1991;Milligan et al, 1991a,b;Leong and Ling, 1992).…”

mentioning

confidence: 96%

Identification of transient microglial cell colonies in the forebrain white matter of developing rats

Earle

Mitrofanis

1997

J. Comp. Neurol.

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Herein, we describe the existence of distinct colonies of transient microglial cells that reside in well-defined zones of the forebrain white matter. Rats, aged at postnatal day (P) 0, P2, P5, P7, P10, P15 or adult, were anaesthetised with halothane gas, and various neural centres were injected unilaterally with the tracer biotinylated Dextran. The neural centres injected were cingulate or sensorimotor cortices, ventral nuclei of the dorsal thalamus, and the pontine reticular formation of the brainstem. Rats were allowed to survive to various stages, from 4 hours to 21 days, after the injection. They were then anaesthetised with sodium pentobarbitone, and their brains were aldehyde-fixed and processed by using standard methods. The following is a description of what is seen after injections at P0, P2, P5, P7, P10; we saw no labelled cells (described below) in the rats injected at P15 or adult. From 2 to 21 days after an injection of dextran into the above-mentioned centres, labelled microglial cell colonies, identified by using double-labelling with anti-OX-6 or Griffonia simplicifolia (Bandeiraea; isolectin B4), were seen in small isolated zones in the forebrain white matter. These colonies were in the corpus callosum, the dorsal and ventral regions of the external capsule, and the internal capsule. A striking feature of these labelled microglial cell colonies was that they were seen on both sides of the brain. Thus, regardless of the location of the injection site in either the cortex, thalamus, or brainstem, the same microglial cell colonies were labelled with dextran in the forebrain white matter. After injections of different coloured fluorescent dextrans into the cortex and into the brainstem of the same animal, many double-labelled cells in each of the colonies were seen. From our short-term survival cases (4 hours to 1 day), a rather strict sequence or progression of labelling of the colonies across the white matter from the injection site was seen; in general, the microglial cell colonies closest to the injection site became labelled well before (about a day) those further away. These results lead us to suggest that the microglial cells in each colony become labelled after a slow diffusion of the tracer through the extracellular space from the injection site.

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Amoeboid and ramified microglia: Their interrelationship and response to brain injury

Cited by 117 publications

References 27 publications

The origin and differentiation of microglial cells during development

The origin and differentiation of microglial cells during development

Microglial response to N-methyl-D-aspartate-mediated excitotoxicity in the immature rat brain

Identification of transient microglial cell colonies in the forebrain white matter of developing rats

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