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Table of Contents
Vol. 17, No. 1, 2010
Issue release date: October 2009
Section title: Original Paper
Neuroimmunomodulation 2010;17:31–38
(DOI:10.1159/000243083)

Kainic Acid-Activated Microglia Mediate Increased Excitability of Rat Hippocampal Neurons in vitro and in vivo: Crucial Role of Interleukin-1beta

Zheng H.a, c · Zhu W.a · Zhao H.a · Wang X.a · Wang W.b · Li Z.a
aDepartment of Brain Research, Division of Anatomy, Tongji Medical College, and bDepartment of Neurology of Tongji Hospital, Huazhong University of Science and Technology, Wuhan, and cDepartment of Biochemistry and Molecular Biology, Xianning College, Xianning, China

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: January 21, 2009
Accepted: March 02, 2009
Published online: October 05, 2009
Issue release date: October 2009

Number of Print Pages: 8
Number of Figures: 5
Number of Tables: 1

ISSN: 1021-7401 (Print)
eISSN: 1423-0216 (Online)

For additional information: http://www.karger.com/NIM

Abstract

Objective: It is known that highly activated microglia and the consequent production of inflammatory cytokines were associated with neuroexcitotoxic injuries. The present study was carried out to explore whether interleukin-1β (IL-1β), a proinflammatory cytokine produced in abundance by activated microglia, mediates increased excitability of hippocampal neurons and the related molecular mechanisms. Methods: Primary cultured microglia were activated by kainic acid (KA), and the KA-treated microglial conditioned medium (KA-MCM) was collected. KA-MCM with or without anti-rat IL-1β monoclonal neutralizing antibody was then injected into the rat in the right cerebral ventricle, or primary cultured hippocampal neurons were treated with the above-mentioned KA-MCM. The population spike amplitude changes in the CA3 region were assessed by electrophysiological recording in vivo. Western blot and RT-PCR assay were performed to investigate the expression changes of N-methyl-D-aspartate receptor subunit 1 (NMDAR1) and inducible nitric oxide synthase (iNOS) expression in hippocampal neurons. Results: Primary cultured microglia were significantly activated by KA with increased IL-1β levels. Interestingly, intracerebroventricular administration of KA-MCM to rats resulted in enhancement of population spike amplitude in the CA3 region and in upregulation of NMDAR1 and iNOS expression in the hippocampus, which was partially attenuated by anti-rat IL-1β antibody. Furthermore, the changes in NMDAR1 and iNOS expression in the rat hippocampus were verified by incubation of primary cultured hippocampal neurons with KA-MCM. Conclusion: This study provides evidence that KA-activated microglia mediate increased excitability of hippocampal neurons in vitro and in vivo and that IL-1β may be one of the main causes of this event.

© 2009 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: January 21, 2009
Accepted: March 02, 2009
Published online: October 05, 2009
Issue release date: October 2009

Number of Print Pages: 8
Number of Figures: 5
Number of Tables: 1

ISSN: 1021-7401 (Print)
eISSN: 1423-0216 (Online)

For additional information: http://www.karger.com/NIM


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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