Quantitative cytoarchitectonic distribution of neurons, glia, and DNA in rat cerebral cortex

Bass, Norman H.; Hess, Helen H.; Pope, Alfred; Thalheimer, Caroline

doi:10.1002/cne.901430405

Cited by 126 publications

(76 citation statements)

References 27 publications

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“…The scenario depicted in Figure 10C would be consistent both with an initial report that some astrocytes are larger in human than in mouse cerebral cortex [86], and the evidence that oligodendrocytes are the predominant glial cell type in the cerebral cortex, at least in some species [81,[83][84][85].…”

Section: Relative Frequencies Of Glial Cell Subtypessupporting

confidence: 88%

“…While many researchers expect or indeed assume that astrocytes are the most common of all glial cell types [43][44][45]82], there is quantitative evidence to the contrary: in the human cerebral cortical gray matter, oligodendrocytes represent about 75% of all glial cells, and astrocytes are only about 20% [81]. Similarly, many other studies on the rat cerebral cortex found that oligodendrocytes constitute the majority of the glial cell population [83][84][85]. In this scenario, the average size of each glial subtype remains constant across structures and species.…”

Section: Relative Frequencies Of Glial Cell Subtypesmentioning

confidence: 98%

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You Do Not Mess with the Glia

Herculano‐Houzel

Santos

2018

Neuroglia

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Vertebrate neurons are enormously variable in morphology and distribution. While different glial cell types do exist, they are much less diverse than neurons. Over the last decade, we have conducted quantitative studies of the absolute numbers, densities, and proportions at which non-neuronal cells occur in relation to neurons. These studies have advanced the notion that glial cells are much more constrained than neurons in how much they can vary in both development and evolution. Recent evidence from studies on gene expression profiles that characterize glial cells-in the context of progressive epigenetic changes in chromatin during morphogenesis-supports the notion of constrained variation of glial cells in development and evolution, and points to the possibility that this constraint is related to the late differentiation of the various glial cell types. Whether restricted variation is a biological given (a simple consequence of late glial cell differentiation) or a physiological constraint (because, well, you do not mess with the glia without consequences that compromise brain function to the point of rendering those changes unviable), we predict that the restricted variation in size and distribution of glial cells has important consequences for neural tissue function that is aligned with their many fundamental roles being uncovered.

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Section: Relative Frequencies Of Glial Cell Subtypessupporting

confidence: 88%

Section: Relative Frequencies Of Glial Cell Subtypesmentioning

confidence: 98%

You Do Not Mess with the Glia

Herculano‐Houzel

Santos

2018

Neuroglia

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“…4). Morphine-dependent morphologic changes in the group of astrocytes with an exaggerated increase in area did not resemble what is typically described as "stellation" (see ref 1), but were similar to changes observed in reactive astrocytes. Lastly, the opioiddependent changes in astrocyte morphology appear to be specific, since dynorphin (a preferential κ-opioid receptor agonist) has no effect on the morphology of cultured pituicytes (GFAP-positive pituitary cells) 2 .…”

Section: Discussionmentioning

confidence: 52%

Morphine alters astrocyte growth in primary cultures of mouse glial cells: evidence for a direct effect of opiates on neural maturation

Stiene‐Martin

Gurwell

Hauser

1991

Developmental Brain Research

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SUMMARYTo determine whether exogenous opiate drugs with abuse liability directly modify neural growth, the present study investigated the effects of morphine on astrocyte proliferation and differentiation in primary cultures of murine glial cells. The results indicate that morphine decreases glial cell production in a dose-dependent, naloxone reversible manner. Most notably, gliogenesis virtually ceased in the presence of 10 −6 M morphine during the first week in culture, whereas 10 −8 M or 10 −10 M morphine caused an intermediate suppression of growth compared to control or 10 −6 M morphine treated cultures. Moreover, morphine-treatment inhibited [ 3 H]thymidine incorporation by glial fibrillary acidic protein (GFAP) immunoreactive, flat (type 1) astrocytes, suggesting that the decrease in glial cell production was due in part to an inhibition of astrocyte proliferation. Morphine also caused significant increases in both cytoplasmic area and process elaboration in flat (type 1) astrocytes indicating greater morphologic differentiation. In the above experiments, morphine-dependent alterations in astrocyte growth were antagonized by naloxone, indicating that morphine action was mediated by specific opioid receptors. These observations suggest that opiate drugs can directly modify neural growth by influencing two critical developmental events in astrocytes, i.e., inhibiting proliferation and inducing morphologic differentiation.

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“…4C, small arrowhead). At 24 hr after ischemia and reperfusion, mRNA levels were highly increased in cells with round large nuclei, presumably neurons (Bass et al, 1971), and oval small nuclei but were reduced in cerebral microvessels (Fig. 4 D,E).…”

Section: Increased Expression Of Mt-1 Mrna and Protein In Microvasculmentioning

confidence: 94%

“…4C, arrow) of the ischemic cortex. Some cells with oval small-sized nuclei, indicative of astrocytes (Bass et al, 1971), showed selective expression of MT-1 mRNA (Fig. 4C, small arrowhead).…”

Section: Increased Expression Of Mt-1 Mrna and Protein In Microvasculmentioning

confidence: 99%

Increased Binding Activity at an Antioxidant-Responsive Element in the Metallothionein-1 Promoter and Rapid Induction of Metallothionein-1 and -2 in Response to Cerebral Ischemia and Reperfusion

Campagne¹,

Thibodeaux²,

Bruggen³

et al. 2000

J. Neurosci.

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Metallothioneins (MTs) are cysteine-rich metal-binding proteins that are potentially involved in zinc homeostasis and free radical scavenging. The expression pattern of MT-1 and the binding activity of various MT-1 promoter elements were investigated after mild focal cerebral ischemia in the rat. Transient focal ischemia was induced by occluding both common carotid arteries and the right middle cerebral artery for 30 min. By the use of real-time quantitative PCR, a 10-fold increase in MT-1 and -2 mRNA levels was found in the cortex 24 hr after reperfusion. In situ hybridization and immunocytochemistry showed a rapid increase in MT-1 and -2 mRNA and MT protein in endothelial cells of microvessels at 6 hr after reperfusion, followed by an increased expression in astrocytes of the infarcted cortex at 24 hr after reperfusion. The early increase in MT expression preceded an increase in cerebral edema measured with T2-weighted magnetic resonance imaging. Gel shift assays were performed on nuclear extracts prepared from cortices before and at 6 and 24 hr after reperfusion. Increased binding activity was found at an antioxidant/electrophilic response element (ARE) sequence in the MT-1 promoter at 6 hr with a lower and variable binding activity at 24 hr after reperfusion. Constitutive binding activity was found for Sp1 and a metal response element in the MT-1 promoter that did not increase after ischemia and reperfusion. This study suggests a role of ARE-binding proteins in inducing cerebral MT-1 expression and implicates MT-1 as one of the early detoxifying genes in an endogenous defense response to cerebral ischemia and reperfusion.Key words: antioxidant response element; cerebral ischemia; edema; electrophoretic mobility shift assay; magnetic resonance imaging; metallothionein; promoter Transient focal cerebral ischemia of 1-2 hr duration induces increased transcription of various genes that either serve to protect cells against the consequences of the insult or activate a cell death pathway (Koistinaho and Hokfelt, 1997). Gene expression is profound in the infarct border zone rather than in the infarct core areas where gene transcription and translation are suppressed and cells die rapidly (Akins et al., 1996). In contrast to focal ischemic insults, global cerebral ischemia elicits a pathology with a clearly delayed time course, and here the gene expression patterns are found in the affected areas before overt pathology (Massa et al., 1996). In the present study we used a model of mild focal cerebral ischemia, in which cell death progresses in a delayed manner (Du et al., 1996;van Lookeren Campagne et al., 1999b). The extended time course of infarct development in this model may resemble the situation in a subset of patients with acute stroke (Pantano et al., 1999) and allows us to study gene expression patterns that potentially fulfill a role early in infarct development. Among the early response genes are metallothionein-1 and -2 (MT-1 and -2). These genes belong to the phase II-responsive detoxifying genes that co...

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Quantitative cytoarchitectonic distribution of neurons, glia, and DNA in rat cerebral cortex

Cited by 126 publications

References 27 publications

You Do Not Mess with the Glia

You Do Not Mess with the Glia

Morphine alters astrocyte growth in primary cultures of mouse glial cells: evidence for a direct effect of opiates on neural maturation

Increased Binding Activity at an Antioxidant-Responsive Element in the Metallothionein-1 Promoter and Rapid Induction of Metallothionein-1 and -2 in Response to Cerebral Ischemia and Reperfusion

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