Chronic gliosis induced by loss of S-100B: Knockout mice have enhanced GFAP-immunoreactivity but blunted response to a serotonin challenge

Matthew S. Chang, Lisa M. Ariah, Alexander Marks, Efrain C. Azmitia

Research output: Contribution to journalArticlepeer-review

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 (-/-).

Original languageEnglish (US)
Pages (from-to)1-9
Number of pages9
JournalBrain Research
Volume1031
Issue number1
DOIs
StatePublished - Jan 7 2005

Keywords

  • Astrocyte
  • Hippocampus
  • Serotonin

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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