Induction of astroglial gene expression by experimental seizures in the rat: Spatio‐temporal patterns of the early stages

Belluardo, Natale; Mudó, G.; Jiang, Xiang-Yu; Condorelli, D. F.

doi:10.1002/(sici)1098-1136(199602)16:2<174::aid-glia9>3.3.co;2-s

Cited by 9 publications

(10 citation statements)

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“…This glial hypertrophy was observed in the light microscopic preparations and was also shown convincingly in electron microscopic images obtained from the hilus at all of the time points examined. The appearance of hypertrophied processes with large bundles of glial filaments as early as one day after seizures would presumably be preceded by increased GFAP mRNA, which can be seen in some regions of the hippocampus as early as 1.5 hrs after pilocarpine‐induced seizures (Belluardo et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Rapid astrocyte and microglial activation following pilocarpine‐induced seizures in rats

2008

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SUMMARYAstrocyte and microglial activation occurs following seizures and plays a role in epileptogenesis. However, the precise temporal and spatial response to seizures has not been fully examined. The pilocarpine model of temporal lobe epilepsy was selected to examine glial changes following seizures because morphological changes in the hippocampus closely mimic the human condition. Astrocytic and microglial changes in the hippocampus were examined during the first 5 days after pilocarpine-induced seizures in rats by analyzing GFAP, Iba1 and S100B-immunolabeling in CA1, CA3, and the hilus. Also, 3-dimensional reconstructions of microglial cells from the hilus and granule cell layer were analyzed. Lastly, astrocyte hypertrophy was examined in the hilus using electron microscopy. At 1 day after seizures and continuing throughout the 5 days examined, hypertrophied Iba1-labeled microglial cells and glial fibrillary acidic protein (GFAP)-labeled astrocytes were observed. At 1 and 2 days after seizures, significantly greater Iba1 immunolabeling was observed in CA1, CA3, and the hilus. In addition, both the area of Iba1 labeled processes and the number of their endings were increased in the hilus beginning at 1 day after seizures. S100B-immunolabeling was significantly elevated in CA3 at 1 day, in CA3 and CA1 at 2 days, and in all three hippocampal regions at 3 days after seizures. Electron microscopy confirmed astrocytic hypertrophy and demonstrated astrocytic cell bodies in the location where glial endfeet normally appear on capillaries. The differential response patterns of astrocytes and microglial cells following pilocarpine-induced seizures may signify their detrimental role in neuroinflammation after seizures.

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Section: Discussionmentioning

confidence: 99%

Rapid astrocyte and microglial activation following pilocarpine‐induced seizures in rats

2008

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“…In recent years, studies strongly suggested a role for inflammation in the pathogenesis of epilepsy. Rapid glial activation has been observed in the adult and immature brain following seizure activity (Khurgel et al., 1995; Belluardo et al., 1996; Taniwaki et al., 1996; Vezzani et al., 2002; Rizzi et al., 2003; Ravizza et al., 2005). Cytokine neosynthesis is induced by seizure in an age‐dependent manner (Rizzi et al., 2003; Ravizza et al., 2005).…”

Section: Discussionmentioning

confidence: 99%

Protective effects of naloxone in two‐hit seizure model

Yang

et al. 2010

Epilepsia

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SUMMARYPurpose: Early life status epilepticus (SE) could enhance the vulnerability of the immature brain to a second SE in adulthood (two-hit seizure model). Naloxone has been proved to possess inflammation inhibitory effects in nervous system. This study was designed to evaluate the dosedependent protective effects of naloxone in kainic acid (KA)-induced two-hit seizure model. Methods: After KA-induced SE at postnatal day 15 (P15), Sprague-Dawley rats were infused with either saline or different doses (1.92, 3.84, 5.76, and 7.68 mg/kg) of naloxone continuously for 12 h. De novo synthesis of cytokines (interleukin-1b [IL-1b], S100B) was assessed by real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) at 12 h after P15 SE. Glial activation states were analyzed by western blotting of glial markers (glial fibrillary acidic protein[GFAP], S100B, Iba1) both at 12 h after P15 SE and at P45. After a second SE at P45, cognitive deteriorations were evaluated by Morris water tests and neuron injuries were evaluated by TdTmediated dUTP nick end labeling (TUNEL) assays. Results: Naloxone reduced IL-1b synthesis and microglial activation most potently at a dose of 3.84 mg/kg. Attenuation of S100B synthesis and astrocyte activation were achieved most dramatically by naloxone at a dose of 5.76 mg/kg, which is equal to the most powerful dose in ameliorating cognitive injuries and neuron apoptosis after second SE. Conclusions: Naloxone treatment immediately after early life SE could dose-dependently reduce cytokine production, glial activation, and further lower the vulnerability of immature brains to a second hit in adulthood.

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“…Both the time course of the phenomenon and the localization of Cx43‐ and Cx32‐expressing cells suggest the possible involvement of reactive glial cells. Indeed, the well‐know localization of Cx43 in astrocytes and the similarity of spatio‐temporal expression patterns of Cx43 mRNA with those of GFAP mRNA (Belluardo et al ., 1996) are in favour of a role of reactive astrocytes. The up‐regulation of Cx43 in reactive astrocytes has been previously reported in other brain injury models (Theriault et al ., 1997; Rami et al ., 2001), and in temporal cortex of patients exhibiting seizures disorders (Naus et al ., 1991).…”

Section: Discussionmentioning

confidence: 99%

Cellular expression of connexins in the rat brain: neuronal localization, effects of kainate‐induced seizures and expression in apoptotic neuronal cells

Condorelli

Trovato‐Salinaro

Mudò

et al. 2003

Eur J of Neuroscience

130

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The identification of connexins (Cxs) expressed in neuronal cells represents a crucial step for understanding the direct communication between neurons and between neuron and glia. In the present work, using a double-labelling method combining in situ hybridization for Cx mRNAs with immunohistochemical detection for neuronal markers, we provide evidence that, among cerebral connexins (Cx26, Cx32, Cx36, Cx37, Cx40, Cx43, Cx45 and Cx47), only Cx45 and Cx36 mRNAs are localized in neuronal cells in both developing and adult rat brain. In order to establish whether connexin expression is influenced in vivo by abnormal neuronal activity, we examined the short-term effects of kainate-induced seizures. The results revealed an unexpected expression of Cx26 and Cx45 mRNA in neuronal cells undergoing apoptotic cell death in the CA3-CA4, in the hilus of the hippocampus and in other brain regions involved in seizure-induced lesion. However, the expression of Cx26 and Cx45 mRNAs was not associated with detectable expression of corresponding proteins as evaluated by immunohistochemistry with specific antibodies. Moreover, in the same brain regions Cx32 and Cx43 were up-regulated in non-neruronal cells whereas the neuronal Cx36 was down-regulated. Taken together the present results provide novel information regarding the specific subpopulation of neurons expressing Cx45 and raise the question of the meaning of connexin mRNA expression in the neuronal apoptotic process.

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Induction of astroglial gene expression by experimental seizures in the rat: Spatio‐temporal patterns of the early stages

Cited by 9 publications

References 0 publications

Rapid astrocyte and microglial activation following pilocarpine‐induced seizures in rats

Rapid astrocyte and microglial activation following pilocarpine‐induced seizures in rats

Protective effects of naloxone in two‐hit seizure model

Cellular expression of connexins in the rat brain: neuronal localization, effects of kainate‐induced seizures and expression in apoptotic neuronal cells

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