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• W1973463271 abstract "Serotonin (5-HT) can induce a release of intraglial S-100B and produce a change in glial morphology. Because S-100B can inhibit polymerization of glial fibrillary acidic protein (GFAP), we hypothesize that glial reactivity may reflect the loss of intraglial S-100B. Adult male transgenic S-100B homozygous knockout (−/−) mice (KO) and wild-type CD-1 (WT) mice were studied. S-100B-immunoreactivity (IR) was seen in the brain tissue of WT (CD-1) but not S-100B KO (−/−) mice. GFAP-IR was seen in both WT (CD-1) and S-100B KO (−/−) glia cells, but S-100B KO (−/−) GFAP-IR cells appeared larger, darker, and more branched than in WT (CD-1). To compare the response of GFAP-IR cells to 5-HT in S-100B KO (−/−) and WT (CD-1) mice, we injected animals with para-chloroamphetamine (PCA) over 2 days (5 and 10 mg/ml). PCA is a potent 5-HT releaser which can induce gliosis in the rodent brain. In WT (CD-1) mice, the size, branching, and density of GFAP-IR cells were significantly increased after PCA injections. No increase in GFAP-IR activation was seen in the S-100B KO (−/−) after PCA injections. Cell-specific densitometry (set at a threshold of 0–150 based on a scale of 255) in these animals statistically showed an increase in GFAP-IR after PCA injections in WT (CD-1) but not S-100B KO (−/−) mice. These results are consistent with the hypothesis that 5-HT may modulate glial morphology by inducing a release of intracellular S-100B, and this pathway is inoperable in the S-100B KO (−/−)." @default.
• W1973463271 created "2016-06-24" @default.
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• W1973463271 date "2005-01-01" @default.
• W1973463271 modified "2023-09-25" @default.
• W1973463271 title "Chronic gliosis induced by loss of S-100B: knockout mice have enhanced GFAP-immunoreactivity but blunted response to a serotonin challenge" @default.
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• W1973463271 doi "https://doi.org/10.1016/j.brainres.2004.07.043" @default.
• W1973463271 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15621007" @default.
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