Acidic pH rapidly increases immunoreactivity of glial fibrillary acidic protein in cultured astrocytes

Oh, Tae Hwan; Markelonis, George J.; Visger, J. R. Von; Baik, Bong Soo; Shipley, Michael T.

doi:10.1002/glia.440130408

Cited by 30 publications

(27 citation statements)

References 12 publications

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“…As the half-life of GFAP is about 7-8 days, neither the rapid increases (1 hour) nor the rapid decreases (,8 hours) of GFAP favors the notion that the increased staining observed here is primarily the result of newly synthesized GFAP (Morrison et al, 1985). Further, we recently reported that cultured astrocytes have increased GFAP staining within 1 hour following decreased pH (Oh et al, 1995), a time course remarkably similar to that seen in the present seizure model. This rapid increase of GFAP was obtained with actinomycin added to the cultures, further indicating that increased staining was not dependent upon translation.…”

Section: Astrocytessupporting

confidence: 83%

“…Consistent with the possibility that local pH could serve as one signal to astrocytes, we have shown that decreased pH (6.0) causes a rapid increase in GFAP staining in cultured astrocytes (Oh et al, 1995). The time course of this GFAP increase corresponds to that observed in the present in vivo experiments.…”

Section: Astrocytessupporting

confidence: 81%

“…During seizures, increased neuronal activity could cause increased K 1 release, which could, in turn, signal the activation of astrocytes and increased GFAP. Interestingly, however, large increases in extracellular K 1 (150 mM) had no effect on GFAP staining in our glial culture model (Oh et al, 1995).…”

Section: Astrocytesmentioning

confidence: 95%

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Soman-induced seizures rapidly activate astrocytes and microglia in discrete brain regions

1997

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Neurons in the piriform cortex and the pontine nucleus locus coeruleus express elevated levels of the immediate early gene protein product, Fos, within 30-45 minutes of a seizurogenic dose of the anticholinesterase, soman (Zimmer et al., [1997] J. Comp. Neurol. 378:468-481). By 24 hours following soman injection, there is marked neuropathology in the piriform cortex. These findings suggest selective, regional vulnerability in response to the seizurogenic actions of soman. In the present study, we determined that soman-induced seizures also cause selective, rapid activation of astrocytes and microglia in the piriform cortex and other brain regions. Animals were killed at different intervals between 1 hour and 24 hours after a convulsive dose of soman. Brain sections were processed for immunocytochemical detection of astrocytes with antibodies against glial fibrillary acidic protein, and microglia and macrophages with antibodies against the complement receptor 3 protein, OX-42. The results demonstrate that following soman administration: (1) there is a rapid increase in glial fibrillary acidic protein staining in astrocytes of the piriform cortex (1 hour); (ii) reactive astrocytes are specifically restricted to layer II and the superficial boundaries of layer III of the piriform cortex. These are the same layers in which neurons express Fos within 30-45 minutes following soman administration; (3) between 1 and 4 hours, resting (ramified) microglia in the piriform cortex and the hippocampus alter their morphology to resemble active microglia. From 4-8 hours, active microglia undergo morphological changes characteristic of reactive microglia that resemble macrophages. Taken together, these observations indicate that astrocytes and microglia in brain regions susceptible to soman become rapidly "reactive" in response to seizures. The highly specific anatomical codistribution of reactive glia and Fos-expressing neurons suggests that intensely active neurons provide local signals that trigger reactive changes in neighboring glia.

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Section: Astrocytessupporting

confidence: 83%

Section: Astrocytessupporting

confidence: 81%

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Soman-induced seizures rapidly activate astrocytes and microglia in discrete brain regions

1997

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“…Differences in the intensity or number of GFAP positive cells were not evident when anti-GFAP was used at a dilution of 1:20,000 (not shown). To enhance possible differences between wild type and mutant brains, the concentration of the polyclonal anti-GFAP antibody was reduced to 1:100,000 [39,45]. At this dilution, the anti-GFAP antibody labeled few cells in control mouse brains.…”

Section: Gfap Expression In Wild Type and Nf1/nf1 Brainsmentioning

confidence: 99%

Region-specific astrogliosis in brains of mice heterozygous for mutations in the neurofibromatosis type 1 (Nf1) tumor suppressor

et al. 1999

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Brains from human neurofibromatosis type 1 (NF1) patients show increased expression of glial fibrillary acidic protein (GFAP), consistent with activation of astrocytes (M.L. Nordlund, T.A. Rizvi, C.I. Brannan, N. Ratner, Neurofibromin expression and astrogliosis in neurofibromatosis (type 1) brains, J. Neuropathol. Exp. Neurology 54 (1995) 588-600). We analyzed brains from transgenic mice in which the Nf1 gene was targeted by homologous recombination. We show here that, in all heterozygous mice analyzed, there are increased numbers of astrocytes expressing high levels of GFAP in medial regions of the periaqueductal gray and in the nucleus accumbens. More subtle, but significant, changes in the number of GFAP positive astrocytes were observed in the hippocampus in 60% of mutant mice analyzed. Astrocytes with elevated GFAP were present at 1 month, 2 months, 6 months and 12 months after birth. Most brain regions, including the cerebellum, basal ganglia, cerebral cortex, hypothalamus, thalamus, cortical amygdaloid area, and white matter tracts did not show any gliotic changes. No evidence of degenerating neurons was found using de Olmos' cupric silver stain. We conclude that Nf1/nf1 mice provide a model to study astrogliosis associated with neurofibromatosis type 1.

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“…This finding is in apparent contradiction to our results showing increases in the staining of GFAP-immunoreactive processes with high [K'l,. It should be noted, however, that changes in the staining and extension of GFAP-immunoreactive processes do not necessarily reflect changes in GFAP synthesis (Aquino et al, 1988;Eng et al, 1989;Oh et al, 1995). GFAP immunoreactivity may increase by the unmasking of antigenic sites a h r a redistribution of intermediate filaments or as a consequence of cell swelling, as well as by posttranslational modifications of GFAP.…”

Section: Discussionmentioning

confidence: 95%

Neurosteroids modulate the reaction of astroglia to high extracellular potassium levels

Cerro

Garcı́a-Estrada

García‐Segura

1996

Glia

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The extracellular concentration of potassium ([K+]0) in brain tissue is modified by neuronal activity and is increased under several pathological conditions. The influence of neurosteroids on the astroglia response to high [K+]0 was assessed on cultured slices from rat hippocampus. Exposure to [K+]0 above physiological (3 mM) levels resulted in the progressive appearance of cell processes immunoreactive for glial fibrillary acidic protein (GFAP). The maximal effect was observed at 50 mM [K+]0, and further increases of [K+]0 did not increase the extension of GFAP‐immunoreactive processes. The effect was observed as early as 10 min after increasing [K+]0, was independent of new protein synthesis, and was reversible, reaching control conditions by 15 h after resetting [K+]0 to physiological levels. Gonadal hormones and neurosteroids had prominent and variable effects on the stimulatory influence of high [K+]0 on astroglia morphology. At physiological [K+]0, 17β‐estradiol and pregnenolone, as well as its sulfate derivative, increased the extension of GFAP‐immunoreactive processes. However, at high [K+]0, testosterone, pregnenolone, and dehydroepiandrosterone and its sulfate derivative decreased the extension of GFAP‐immunoreactive processes. Effects of gonadal hormones and neurosteroids were blocked by the protein synthesis inhibitor cycloheximide. These results suggest that non‐genomic effects of high [K+]0 on glial cells interact with genomic effects of steroids to modulate astroglia morphology. © 1996 Wiley‐Liss, Inc.

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Acidic pH rapidly increases immunoreactivity of glial fibrillary acidic protein in cultured astrocytes

Cited by 30 publications

References 12 publications

Soman-induced seizures rapidly activate astrocytes and microglia in discrete brain regions

Soman-induced seizures rapidly activate astrocytes and microglia in discrete brain regions

Region-specific astrogliosis in brains of mice heterozygous for mutations in the neurofibromatosis type 1 (Nf1) tumor suppressor

Neurosteroids modulate the reaction of astroglia to high extracellular potassium levels

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