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 journalArticle

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

Fingerprint

Gliosis
Glial Fibrillary Acidic Protein
p-Chloroamphetamine
Knockout Mice
Serotonin
Neuroglia
Injections
Densitometry
Brain
Polymerization
Rodentia

Keywords

  • Astrocyte
  • Hippocampus
  • Serotonin

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Chronic gliosis induced by loss of S-100B : Knockout mice have enhanced GFAP-immunoreactivity but blunted response to a serotonin challenge. / Chang, Matthew S.; Ariah, Lisa M.; Marks, Alexander; Azmitia, Efrain C.

In: Brain Research, Vol. 1031, No. 1, 07.01.2005, p. 1-9.

Research output: Contribution to journalArticle

@article{f623fc66deeb406fb8612c8633732df6,
title = "Chronic gliosis induced by loss of S-100B: Knockout mice have enhanced GFAP-immunoreactivity but blunted response to a serotonin challenge",
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 (-/-).",
keywords = "Astrocyte, Hippocampus, Serotonin",
author = "Chang, {Matthew S.} and Ariah, {Lisa M.} and Alexander Marks and Azmitia, {Efrain C.}",
year = "2005",
month = "1",
day = "7",
doi = "10.1016/j.brainres.2004.07.043",
language = "English (US)",
volume = "1031",
pages = "1--9",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - Chronic gliosis induced by loss of S-100B

T2 - Knockout mice have enhanced GFAP-immunoreactivity but blunted response to a serotonin challenge

AU - Chang, Matthew S.

AU - Ariah, Lisa M.

AU - Marks, Alexander

AU - Azmitia, Efrain C.

PY - 2005/1/7

Y1 - 2005/1/7

N2 - 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 (-/-).

AB - 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 (-/-).

KW - Astrocyte

KW - Hippocampus

KW - Serotonin

UR - http://www.scopus.com/inward/record.url?scp=11144251738&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=11144251738&partnerID=8YFLogxK

U2 - 10.1016/j.brainres.2004.07.043

DO - 10.1016/j.brainres.2004.07.043

M3 - Article

C2 - 15621007

AN - SCOPUS:11144251738

VL - 1031

SP - 1

EP - 9

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1

ER -