Selective Increase in S‐100β Protein by Aging in Rat Cerebral Cortex

Kato, Kanefusa; Suzuki, Fujiko; Morishita, Rika; Asano, Taku; Sato, Tsuneko

doi:10.1111/j.1471-4159.1990.tb01958.x

Cited by 59 publications

(21 citation statements)

References 44 publications

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“…In these brain regions, effects of S100 on neuroplasticity have been shown (Lewis and Teyler 1986;Mfiller et al 1993), which in turn may influence S100 immunoreactivity of astrocytes (Haring et al 1993). A special role for S100 in the cerebral cortex is also documented by the increase of S100b in aging rats (Kato et al 1990). Recently, we presented preliminary evidence that patterns of S100 immunoreactivity may vary between different regions of the forebrain and that premortal conditions may modify these distribution patterns of S100 immunoreactivity (Rickmann and Wolff 1992;Laskawi et al 1993).…”

Section: Introductionmentioning

confidence: 92%

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Modifications of S100-protein immunoreactivity in rat brain induced by tissue preparation

Rickmann¹,

Wolff²

1995

Histochem Cell Biol

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Immunocytochemistry using antibodies against various molecular forms of the Ca++ and Zn(++)-binding S100 proteins predominantly labelled astrocytes. However, especially in the neocortex the staining pattern is variable. Methods of tissue preparation have been evaluated with the aim to preserve as much S100 immunoreactivity as possible. Optimal results were obtained after perfusion fixation with 4-5% aldehydes, 0.1 M sodium cacodylate, 0.1% CaCl2, pH 7.3. In such preparations, astrocytes were completely labelled including their lamellar compartments in large parts of the central nervous system. Ca(++)-withdrawal had adverse affects on S100 immunoreactivity. Cryostat sections treated with EDTA-containing solutions before fixation showed that Ca(++)-free S100 can apparently not be fixed to the tissue. Perfusion fixatives containing EDTA resulted in inhomogeneous loss of S100 staining, indicating a differential susceptibility of astrocytic subpopulations. A different type of reduction in S100 immunoreactivity occurred around large neocortical blood vessels. Perivascular defects in immunostaining occasionally appeared even after optimal fixation, but could be regularly provoked by mildly acidic fixation (pH 6.6) or prolonged barbiturate anaesthesia. These defects might be based on S100 release into the cerebrospinal fluid. Presumably under none of the conditions studied can the immunoreactivity of all S100-forms and -fractions be completely preserved in the tissue. However, recommendations are presented for optimizing tissue preparation, to the extent that premortal modifications affecting the stainability of astrocytes may be detected by S100 immunohistochemistry in fixed brain tissue.

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Section: Introductionmentioning

confidence: 92%

“…The relative amounts of S100b and S100a show high interspecies variation, e.g. the rat brain contains more than 95% S 100b (Kato et al 1990). …”

Section: Introductionmentioning

confidence: 98%

Modifications of S100-protein immunoreactivity in rat brain induced by tissue preparation

Rickmann¹,

Wolff²

1995

Histochem Cell Biol

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“…Aging is clearly associated with an increased expression of S100B protein and mRNA in rats (Kato et al, 1990). In senescence-accelerated mice, S100B protein and mRNA is significantly increased (Griffin et al, 1998a).…”

Section: In Vivo Animal Experimentsmentioning

confidence: 99%

S100B in brain damage and neurodegeneration

Rothermundt

Peters

Prehn³

et al. 2003

Microscopy Res & Technique

548

411

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S100B is a calcium-binding peptide produced mainly by astrocytes that exert paracrine and autocrine effects on neurons and glia. Some knowledge has been acquired from in vitro and in vivo animal experiments to understand S100B's roles in cellular energy metabolism, cytoskeleton modification, cell proliferation, and differentiation. Also, insights have been gained regarding the interaction between S100B and the cerebral immune system, and the regulation of S100B activity through serotonergic transmission. Secreted glial S100B exerts trophic or toxic effects depending on its concentration. At nanomolar concentrations, S100B stimulates neurite outgrowth and enhances survival of neurons during development. In contrast, micromolar levels of extracellular S100B in vitro stimulate the expression of proinflammatory cytokines and induce apoptosis. In animal studies, changes in the cerebral concentration of S100B cause behavioral disturbances and cognitive deficits. In humans, increased S100B has been detected with various clinical conditions. Brain trauma and ischemia is associated with increased S100B concentrations, probably due to the destruction of astrocytes. In neurodegenerative, inflammatory and psychiatric diseases, increased S100B levels may be caused by secreted S100B or release from damaged astrocytes. This review summarizes published findings on S100B regarding human brain damage and neurodegeneration. Findings from in vitro and in vivo animal experiments relevant for human neurodegenerative diseases and brain damage are reviewed together with the results of studies on traumatic, ischemic, and inflammatory brain damage as well as neurodegenerative and psychiatric disorders. Methodological problems are discussed and perspectives for future research are outlined.

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“…The immunohistochemical study revealed that striatal protein level of S100β also increased significantly after treatment, indicating that Mn-induced S100β mRNA transcript upregulation was translated. This Mn-induced increase in S100β overexpression is reminiscent of increases in S100β expression that accompany normal aging in both humans 11) and experimental animals 12) . In Alzheimer's disease, there are elevated tissue levels of both biologically active S100β protein and S100β mRNA 13) , and these increases correlated with overexpression of S100β by plaque-associated astrocytes 8,10,14) .…”

Section: Discussionmentioning

confidence: 99%

cDNA Array Analysis of Gene Expression Profiles in Brain of Mice Exposed to Manganese

Baek¹,

Cho²,

Kim³

et al. 2004

INDUSTRIAL HEALTH

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This study is performed to detect changes of gene expression in substantia nigra (SN) and striatum in manganese (Mn)-exposed mice brain. The cDNA array is a recently developed molecular biological method that can detect the differential expression of several hundreds of genes simultaneously and is therefore advantageous in the study of trace metal intoxication effect at the genetic level. Using this technology, we discovered 5 genes in the mouse striatum and 9 genes in SN changed by more than 50% following Mn exposure. Depression were observed in two genes (neural cell adhesion protein BIG2, heavy neurofilament subunit genes) in striatum and three genes (light neurofilament subunit, brain acyl-CoA synthetase II, heavy neurofilament subunit genes) in the SN. However three genes (N-acetylglucosaminyltransferase I, S100β β β β β, and synaptonemal complex protein I genes) in striatum and six genes (noggin, striatin, Ost oncogene, S100β β β β β, calcium/calmodulindependent protein kinase kinase beta, and N-acetylglucosaminyltransferase I genes) in SN were elevated following Mn exposure. Immunohistochemical study revealed that protein levels of S100β β β β β also increased following Mn treatment. Activated astrocytes overexpressing S100β β β β β are invariably and intimately associated with decreased expression of heavy and light neurofilament subunits which is a distinguishing feature of neurodegeneration by Mn exposure. All our findings suggested that neuronal degenerations occur in SN as well as striatum of mice exposed to Mn.

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Selective Increase in S‐100β Protein by Aging in Rat Cerebral Cortex

Cited by 59 publications

References 44 publications

Modifications of S100-protein immunoreactivity in rat brain induced by tissue preparation

Modifications of S100-protein immunoreactivity in rat brain induced by tissue preparation

S100B in brain damage and neurodegeneration

cDNA Array Analysis of Gene Expression Profiles in Brain of Mice Exposed to Manganese

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