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Endothelins regulate astrocyte gap junctions in rat hippocampal slices.

Journal article
Authors Fredrik Blomstrand
L Venance
A-L Sirén
P Ezan
Eric Hanse
J Glowinski
H Ehrenreich
C Giaume
Published in The European journal of neuroscience
Volume 19
Issue 4
Pages 1005-15
ISSN 0953-816X
Publication year 2004
Published at Institute of Clinical Neurosciences
Institute of Physiology and Pharmacology, Dept of Physiology
Pages 1005-15
Language en
Links www.ncbi.nlm.nih.gov/entrez/query.f...
Keywords Animals, Animals, Genetically Modified, Astrocytes, drug effects, physiology, Cells, Cultured, Endothelins, antagonists & inhibitors, deficiency, physiology, Gap Junctions, drug effects, physiology, Hippocampus, drug effects, physiology, Rats, Rats, Wistar, Receptor, Endothelin B, antagonists & inhibitors, deficiency, Sulfonamides, pharmacology
Subject categories Physiology

Abstract

Gap junctional communication (GJC) is a typical feature of astrocytes proposed to contribute to the role played by these glial cells in brain physiology and pathology. In acutely isolated hippocampal slices from rat (P11-P19), intercellular diffusion of biocytin through gap junction channels was shown to occur between hundreds of cells immuno-positive for astrocytic markers studied in the CA1/CA2 region. Single-cell RT-PCR demonstrated astrocytic mRNA expression of several connexin (Cx) subtypes, the molecular constituent of gap junction channels, whereas immunoblotting confirmed that Cx43 and Cx30 are the main gap junction proteins in hippocampal astrocytes. In the brain, astrocytes represent a major target for endothelins (Ets), a vasoactive family of peptides. Our results demonstrate that Ets decrease the expression of phosphorylated Cx43 forms and are potent inhibitors of GJC. The Et-induced effects were investigated using specific Et receptor agonists and antagonists, including Bosentan (Tracleer trade mark ), an EtA/B receptor antagonist, and using hippocampal slices and cultures from EtB-receptor-deficient rats. Interestingly, the pharmacological profile of Ets effects did not follow the classical profile established in cardiovascular systems. The present study therefore identifies Ets as potent endogenous inhibitory regulators of astrocyte networks. As such, the action of these peptides on astrocyte GJC might be involved in the contribution of astrocytes to neuroprotective processes and have a therapeutic potential in neuropathological situations.

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