Autoradiographic investigations of glial proliferation in the brain of adult mice. The DNA synthesis phase of neuroglia and endothelial cells

Korr, Hubert; Schultze, B.; Maurer, W.

doi:10.1002/cne.901500205

Cited by 95 publications

(37 citation statements)

References 31 publications

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“…Inspection of the Z-series sections of the confocal images invariably showed that the BrdU-labeled nucleus and the nucleus of the NeuN-labeled neuron were different. Our results with regard to adult neurogenesis in the frontal cortex are in agreement with earlier work by Korr et al (1973) and recent work by Kornack and Rakic (2001). These reports, using different S-phase markers, failed to show the presence of labeled neurons in cortical areas of mice and monkeys.…”

Section: Discussionsupporting

confidence: 93%

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Electroconvulsive Seizure Treatment Increases Cell Proliferation in Rat Frontal Cortex

Madsén

Yeh

Valentine

et al. 2004

Neuropsychopharmacol

113

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Recent studies have demonstrated increased neurogenesis in adult hippocampus in response to electroconvulsive seizure (ECS) or antidepressant drug treatment. Adult neurogenesis in the subgranular zone of the hippocampus and the subventricular zone is well established, whereas neuronal proliferation outside of these areas under unstimulated conditions is not observed. Since mood disorders are likely to involve brain regions in addition to hippocampus, particularly the frontal cortex, it is likely that antidepressant treatments produce cellular changes in these brain regions as well. In this study, we have investigated the effect of repeated ECS administration on the proliferation of cells in the frontal cortex, and we have examined the phenotype of these cells 4 weeks after labeling with a cell division marker. We found that ECS treatment increases the number of newly divided cells in the frontal cortex and that these new cells express markers of either endothelial cells or oligodendrocytes, but not neurons. It is possible that increased proliferation of these cell types in the frontal cortex could reverse the loss of glial cell number and the reduced volume that has been reported in the frontal cortex of depressed patients.

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Section: Discussionsupporting

confidence: 93%

“…As is the case for oligodendrocytes, endothelial cell proliferation in the brain has been documented previously (Korr et al, 1973;Mares and Bruckner, 1978). The fraction of BrdU-labeled cells with an endothelial phenotype was constant in the two groups.…”

Section: Discussionmentioning

confidence: 62%

Electroconvulsive Seizure Treatment Increases Cell Proliferation in Rat Frontal Cortex

Madsén

Yeh

Valentine

et al. 2004

Neuropsychopharmacol

113

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“…Although only a small percentage of the total glia in the corpora callosa are BrdU ϩ , the total number of newly generated glia is undoubtedly much higher than the numbers suggest. Cells incorporate BrdU only while they are in the S phase of the cell cycle, ϳ6 -8 h for glial cells (Korr et al, 1973). Therefore, several injections spaced over 1 d would be needed to label all proliferating glia in a 24 h interval, and multiple injections over a prolonged period of time would be needed to estimate the total numbers of glia generated in adult rodents.…”

Section: Glia Cell Proliferationmentioning

confidence: 99%

Proliferation and Death of Oligodendrocytes and Myelin Proteins Are Differentially Regulated in Male and Female Rodents

et al. 2006

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Sexual dimorphism of neurons and astrocytes has been demonstrated in different centers of the brain, but sexual dimorphism of oligodendrocytes and myelin has not been examined. We show, using immunocytochemistry and in situ hybridization, that the density of oligodendrocytes in corpus callosum, fornix, and spinal cord is 20 -40% greater in males compared with females. These differences are present in young and aged rodents and are independent of strain and species. Proteolipid protein and carbonic anhydrase-II transcripts, measured by real-time PCR, are approximately two to three times greater in males. Myelin basic protein and 2Ј,3Ј-cyclic nucleotide 3Ј-phosphodiesterase, measured by Western blots, are 20 -160% greater in males compared with females. Surprisingly, both generation of new glia and apoptosis of glia, including oligodendrocytes, are approximately two times greater in female corpus callosum. These results indicate that the lifespan of oligodendrocytes is shorter in females than in males. Castration of males produces a female phenotype characterized by fewer oligodendrocytes and increased generation of new glia. These findings indicate that exogenous androgens differentially affect the lifespan of male and female oligodendrocytes, and they can override the endogenous production of neurosteroids. The data imply that turnover of myelin is greater in females than in males. -Calpain, a protease upregulated in degeneration of myelin, is dramatically increased at both transcriptional and translational levels in females compared with males. These morphological, molecular, and biochemical data show surprisingly large differences in turnover of oligodendrocytes and myelin between sexes. We discuss the potential significance of these differences to multiple sclerosis, a sexually dimorphic disease, whose progression is altered by exogenous hormones.

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“…We suggest that the labeled cells in the cortex are the result of simultaneous retroviral uptake by individual cells induced to proliferate by injury, rather than a group of clonally related cells from a single infection. These injury-induced, proliferating cells are most likely astrocytes and/or microglia (Korr et al, 1973;Lindsay, 1986;Graeber et al, 1988;Morshead and van der Kooy, 1990).…”

Section: Proliferation Kinetics Revealed By Cumulative Brdu Labelingmentioning

confidence: 99%

“…Retroviral labeling permits unequivocal tracing of the progeny of an infected proliferating cell without dilution of the label. 3H-thy and bromodeoxyuridine (BrdU; a thymidine analog) can be used to investigate the cell cycle kinetics of anatomically defined populations in pre-and postnatal animals (Waechter and Jaensch, 1972;Korr et al, 1973;Lewis et al, 1977;Nowakowski et al, 1989). We utilized BrdU in a cumulative labeling protocol to determine the proliferation kinetics of the subependymal cells: (1) the length of the cell cycle (r') and the DNA-synthetic phase (Ts) and (2) the growth fraction (GF), which is the proportion of subependymal cells that comprises the proliferating population.…”

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confidence: 99%

Postmitotic death is the fate of constitutively proliferating cells in the subependymal layer of the adult mouse brain

1992

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The early development of the mammalian forebrain involves the massive proliferation of the ventricular zone cells lining the lateral ventricles. A remnant of this highly proliferative region persists into adult life, where it is known as the subependymal layer. We examined the proliferation kinetics and fates of the mitotically active cells in the subependyma of the adult mouse. The medial edge, the lateral edge, and the dorsolateral corner of the subependymal layer of the rostral portion of the lateral ventricle each contained mitotically active cells, but the dorsolateral region had the highest percentage of bromodeoxyuridine (BrdU)-labeled cells per unit area. Repeated injections of BrdU over 14 hr revealed a proliferation curve for the dorsolateral population with a growth fraction of 33%, indicating that 33% of the cells in this subependymal region make up the proliferating population. The total cell cycle time in this population was approximately 12.7 hr, with an S-phase of 4.2 hr. To examine the fate of these proliferating cells, we injected low concentrations of a replication-deficient, recombinant retrovirus directly into the lateral ventricles of adult mice for uptake by mitotically active subependymal cells. Regardless of the survival time postinjection (10 hr, 1 d, 2 d, or 8 d), the number of retrovirally labeled cells per clone remained the same (1 or 2 cells/clone). This suggests that one of the progeny from each cell division dies. Moreover, the clones remained confined to the subependyma and labeled cells were not seen in the surrounding brain tissue. Thus, while 33% of the dorsolateral subependymal cells continue to proliferate in adult life, the fate of the postmitotic progeny is death.

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Autoradiographic investigations of glial proliferation in the brain of adult mice. The DNA synthesis phase of neuroglia and endothelial cells

Cited by 95 publications

References 31 publications

Electroconvulsive Seizure Treatment Increases Cell Proliferation in Rat Frontal Cortex

Electroconvulsive Seizure Treatment Increases Cell Proliferation in Rat Frontal Cortex

Proliferation and Death of Oligodendrocytes and Myelin Proteins Are Differentially Regulated in Male and Female Rodents

Postmitotic death is the fate of constitutively proliferating cells in the subependymal layer of the adult mouse brain

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