Differential expressions of aquaporin subtypes in astroglia in the hippocampus of chronic epileptic rats

Kim, J.-E.; Ryu, Hea Jin; Yeo, Seong-Il; Seo, Cheong Hoon; Lee, B.C.; Choi, Ihn-Geun; Kim, D.-S.; Kang, Tae‐Cheon

doi:10.1016/j.neuroscience.2009.07.028

Cited by 60 publications

(58 citation statements)

References 56 publications

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“…In epilepsy, astrocytes have been reported to transform into ''reactive astrocytes'' (Belluardo et al, 1996;Hansen et al, 1990;Pollen and Trachtenberg, 1970), which are morphologically characterized by increased volume in humans (Binder and Steinhauser, 2006;de Lanerolle et al, 2010;Kim et al, 2009Kim et al, , 2010 and by disorganized architecture of process tufts and domain overlapping in mice (Oberheim et al, 2008).…”

Section: Is Reactive Astrogliosis Replicated In Thementioning

confidence: 99%

Redistribution of astrocytic glutamine synthetase in the hippocampus of chronic epileptic rats

Papageorgiou

Gabriel

Fetani

et al. 2011

Glia

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Glutamine synthetase (GS) is an astrocytic enzyme, which catalyzes the synthesis of glutamine from glutamate and ammonia. In the central nervous system, GS prevents glutamate-dependent excitotoxicity and detoxifies nitrogen. Reduction in both expression and activity of GS was reported in the hippocampus of patients with temporal lobe epilepsy (TLE), and this reduction has been suggested to contribute to epileptogenesis. In this study, we characterized hippocampal GS expression in the pilocarpine model of TLE in Wistar rats by means of stereology and morphometric analysis. Neither the GS positive cell number nor the GS containing cell volume was found to be altered in different hippocampal subregions of chronic epileptic rats when compared with controls. Instead, redistribution of the enzyme at both intracellular and tissue levels was observed in the epileptic hippocampus; GS was expressed more in proximal astrocytic branches, and GS expressing astrocytic somata was located in closer proximity to vascular walls. These effects were not due to shrinkage of astrocytic processes, as revealed by glial fibrillary acidic protein staining. Our results argue for GS redistribution rather than downregulation in the rat pilocarpine model of TLE. The potential contribution of increased GS perivascular affinity to the pathogenesis of epilepsy is discussed as well.

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Section: Is Reactive Astrogliosis Replicated In Thementioning

confidence: 99%

Redistribution of astrocytic glutamine synthetase in the hippocampus of chronic epileptic rats

Papageorgiou

Gabriel

Fetani

et al. 2011

Glia

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“…Furthermore, we have found TUNELpositive astroglial death in the molecular layer (not the hilus) of the dentate gyrus and the frontoparietal cortex after pilocarpine-induced SE [6,8,9]. In contrast, we have found hypertrophic vacuolized astroglia (clasmatodendrosis) in the stratum radiatum of the CA1 region within the rat hippocampus only in the chronic epileptic state, but not in the acute or latent period after SE [8][9][10]. Furthermore, astroglial damage in the piriform cortex is related to vasogenic edema, since severe serum-protein extravasation ss observed in the layer III/IV [9,11].…”

Section: Introductionmentioning

confidence: 62%

“…Bonferroni's test was used for post-hoc comparisons. A p value below 0.05 was considered statistically significant [10,24].…”

Section: Quantification Of Data and Statistical Analysismentioning

confidence: 99%

The roles of P2X7 receptor in regional-specific microglial responses in the rat brain following status epilepticus

et al. 2011

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Recently, we have reported that astroglial activations in response to status epilepticus (SE) show regional-specific manners in the rat hippocampus. However, it is unknown that microglial responses to SE would show regional-specific patterns. Therefore, the present study was designed to elucidate the regional-specific microglial activation and relationship between P2X7 receptor functions and SE-induced microglial responses in the rat brain. Following SE, microglia appeared amoeboid or phagocytic in the dentate gyrus and the piriform cortex. In contrast, elongated microglia were observed in the CA1 hippocampal regions and the frontoparietal cortex. In the dentate gyrus, the CA1 hippocampal regions, and the frontoparietal cortex, these microglial activation accelerated by BzATP (a P2X7 receptor agonist)-infusion, but inhibited by OxATP (a P2X7 receptor antagonist). However, SE-induced microglial activation in the piriform cortex was not affected by BzATP or OxATP-infusion. Therefore, our findings indicate that SE-induced microglial activation may show regional-specific manners, and suggest that P2X7 receptor function differently modulates SE-induced microglial responses in distinct brain regions.

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“…Kim et al, studied regulation of various AQPs in the rat pilocarpine model of epilepsy (Kim et al, 2009(Kim et al, , 2010. In control animals, AQP4 immunoreactivity was detected diffusely in the piriform cortex and hippocampus, with greatest expression at astrocyte endfeet.…”

Section: Expression and Regulation Of Aqp4 During Epileptogenesismentioning

confidence: 99%

Aquaporin‐4 and epilepsy

Binder

Nagelhus

Ottersen

2012

Glia

142

111

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Recent studies have implicated glial cells in modulation of synaptic transmission, so it is plausible that glial cells may have a functional role in the hyperexcitability characteristic of epilepsy. Indeed, alterations in distinct astrocyte membrane channels, receptors, and transporters have all been associated with the epileptic state. This review focuses on the potential roles of the glial water channel aquaporin-4 (AQP4) in modulation of brain excitability and in epilepsy. We will review studies of mice lacking AQP4 (Aqp4 2/2 mice) or a-syntrophin (an AQP4 anchoring protein) and discuss the available human studies demonstrating alterations of AQP4 in human epilepsy tissue specimens. We will conclude with new studies of AQP4 regulation and discuss the potential role of AQP4 in the development of epilepsy (epileptogenesis). While many questions remain unanswered, the available data indicate that AQP4 and its molecular partners may represent important new therapeutic targets. V

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Differential expressions of aquaporin subtypes in astroglia in the hippocampus of chronic epileptic rats

Cited by 60 publications

References 56 publications

Redistribution of astrocytic glutamine synthetase in the hippocampus of chronic epileptic rats

Redistribution of astrocytic glutamine synthetase in the hippocampus of chronic epileptic rats

The roles of P2X7 receptor in regional-specific microglial responses in the rat brain following status epilepticus

Aquaporin‐4 and epilepsy

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