A transient immunoglobulin-like reactivity in the developing cerebral cortex of rodents

Fairén, Alfonso; Smith-Fernández, Aníbal; Martı́, Elisa; I, DeDiego; Rosa, Enrique J. de la

doi:10.1097/00001756-199210000-00015

Cited by 12 publications

(5 citation statements)

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“…Subplate neurons express Alz-50 immunoreactivity, indicating cell degeneration (Al-Ghoul and Miller, 1989). Loss of subplate cells may be related to the transient immunoglobulin-like reactivity in the subplate (Fairen et al, 1992;Upender et al, 1997). Spreafico and colleagues (1995) have used DNA end labeling techniques to reveal cells undergoing apoptosis and report frequent labeling in the subplate of rats.…”

Section: Neuronal Cell Death In the Subplate Regionmentioning

confidence: 99%

Do subplate neurons comprise a transient population of cells in developing neocortex of rats?

et al. 2000

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Studies were undertaken to determine whether neurons of the subplate layer represent a transient or stable population of cells in developing neocortex of rat. The first set of studies sought to determine the fraction of subplate neurons that is lost during early postnatal development. The optical dissector method was used to analyze fluorescently stained material in animals the age of postnatal day 0 (P0) to P40. These results demonstrate a reduction of slightly less than half of the total number of subplate neurons from P0 to P40. Counts of labeled cells in littermates at varied ages after [(3)H]thymidine or BRDU treatment on gestational day 14 (G14 - birthdate of occipital subplate neurons) or G18 (birthdate of layers III-IV neurons) demonstrate loss of approximately 50% of neurons in the subplate layer between P0 and P40, somewhat greater than the loss of neurons from cortical layers III-IV. The second set of studies investigated whether subplate neurons display cellular atrophy during postnatal development. Analysis of subplate neurons injected intracellularly with Lucifer yellow in fixed slice preparations indicates no reduction in soma size, number of dendrites, or extent of dendritic fields of subplate neurons taken from animals age P0 to P60. The third set of studies investigated whether functional markers of subplate neurons are reduced during postnatal development. Analysis of tissue stained histochemically for cytochrome oxidase or acetylcholinesterase, or stained immunocytochemically for GABA, somatostatin, or neuropeptide Y, demonstrate a remarkable loss of expression of staining patterns from late gestational ages to P20. These data demonstrate that, although subplate neurons seem not to be a transient population of cells in the usual sense of being eliminated by cell death or structural atrophy, the loss of histochemical and immunocytochemical markers indicates that they may be a functionally transient population of cells.

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Section: Neuronal Cell Death In the Subplate Regionmentioning

confidence: 99%

Do subplate neurons comprise a transient population of cells in developing neocortex of rats?

et al. 2000

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“…These proteins are expressed on astrocytes, ependymal cells, endothelial cells, microglia and neurons [reviewed in Barnum, 1995]. IgG molecules are also present within the developing nervous system, where they are selectively taken up by immature neurons in the cerebral cortex, midbrain, retina, and cerebellum [Naegele et al, 1991;Fairen et al, 1992;Henschel and Wahle, 1994;Dunn et al, 1995;Upender et al, 1997;Weiner and Chun, 1997].…”

Section: Introductionmentioning

confidence: 99%

Activation of Microglia during Developmentally Regulated Cell Death in the Cerebral Cortex

Upender

Naegele²

1999

Dev Neurosci

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Neuronal elimination in the developing CNS is accomplished by an orderly type of cellular suicide called programmed cell death. The principal non-neuronal cells implicated in regulating programmed cell death and subsequent phagocytosis of dying neurons are the brain’s macrophage population, the microglia. Little is known about the signaling between microglia and neurons during programmed cell death. However, macrophages in non-neural tissues express receptors for immunoglobulin (IgG) and complement, and these molecules help regulate phagocytosis of dying cells and foreign organisms. Since many of the neurons generated early in CNS development are transient cell types that are immunoreactive for IgG [Upender et al.: J Comp Neurol 1997; 384:271–282], we hypothesized that IgG might alter the phagocytic properties of microglia within the developing nervous system and potentiate engulfment of dying cells. To begin to address this hypothesis, we first asked whether cortical neurons immunoreactive for IgG or calbindin-D28k exhibit morphological evidence of programmed cell death in the cerebral cortex of neonatal rat pups. Secondly, we quantified the incidence of contacts made by microglia on IgG- vs. calbindin-immunoreactive neurons. Thirdly, perturbation experiments were performed to elevate intracortical levels of IgG and the incidence of microglia:neuron contacts were determined. We found that although the nuclei of some IgG-immunoreactive neurons exhibited condensation and fragmentation characteristic of programmed cell death, we did not observe pyknotic calbindin-immunoreactive neurons. IgG-immunoreactive neurons were also more likely to be contacted by microglia than calbindin-immunoreactive neurons. Elevating intracortical levels of IgG experimentally led to a dramatic increase in the expression of microglia complement receptors throughout the cerebral cortex. Taken together, these results suggest that IgG normally present within neuronal subsets in the developing cerebral cortex could serve to locally regulate the expression of complement receptors on microglia.

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“…In adult intact rats, for example, IgG‐like immunoreactivity was found in neurons of certain brain nuclei, as best represented by motor neurons in the brainstem and spinal cord (Fabian and Ritchie, 1986; Yamamoto et al, 1987). In perinatal infant rodents (rats and mice), immunoglobulin‐like staining was observed in subplate neurons of the developing cerebral cortex (Fairen et al, 1992; Upender et al, 1997). In aged human brains with or without Alzheimer's disease, occasional neurons or glia, or both, particularly those located in perivascular regions, were reportedly stained for IgG‐like immunoreactivity (Ishii et al, 1975; Mann et al, 1982; Mori et al, 1991).…”

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confidence: 99%

Mouse brain IgG‐like immunoreactivity: Strain‐specific occurrence in microglia and biochemical identification of IgG

Hazama¹,

Yasuhara²,

Morita³

et al. 2005

J of Comparative Neurology

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Unlike the brains of most mammals, the mouse brain appears unique in the massive appearance of cells showing IgG-like immunoreactivity, which has repeatedly been shown via immunohistochemistry. In the present study, we first examined possible species differences in IgG-like immunohistochemical staining in the brains of various rodents, including mice. In four of six mouse strains examined (ICR, Balb/c, C57BL/6, and AKR/J), antibodies against mouse IgG revealed positive staining in many brain microglia. However, no such positive staining was detected in brains of the rat, hamster, guinea pig, or two other mouse strains (CBA/N and CBA/J). We purified IgG-like-immunoreactive molecule(s) biochemically from brain of the ICR mouse as a representative mouse strain. Our amino-acid-sequence analysis proved that the purified protein was identical to serum IgG. The possibility of IgG synthesis by brain microglia in the ICR mouse was denied by our RT-PCR experiments and in situ hybridization histochemistry. In addition, Fcgamma-receptor-deficient double-knockout mice of the C57BL/6 genetic background contained no IgG-immunoreactive microglia in the brain. These results clearly indicate that microglial IgG staining is due to the uptake of serum IgG through Fcgamma receptors. However, the strain-specific mechanisms resulting in microglial IgG uptake remain to be elucidated, in that Fcgamma receptors are omnipresent in microglia of all rodents examined here.

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A transient immunoglobulin-like reactivity in the developing cerebral cortex of rodents

Cited by 12 publications

References 0 publications

Do subplate neurons comprise a transient population of cells in developing neocortex of rats?

Do subplate neurons comprise a transient population of cells in developing neocortex of rats?

Activation of Microglia during Developmentally Regulated Cell Death in the Cerebral Cortex

Mouse brain IgG‐like immunoreactivity: Strain‐specific occurrence in microglia and biochemical identification of IgG

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