Age-dependent neuroinflammatory responses and deficits in long-term potentiation in the hippocampus during systemic inflammation

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• 作者：X. Liu^a ; Z. Wu^a ; ^{zhouw@dent.kyushu-u.ac.jp} ; Y. Hayashi^a ; H. Nakanishi^a ; ^b ; ^{nakan@dent.kyushu-u.ac.jp}
• 关键词：AA ; adjuvant arthritis ; ACSF ; artificial cerebrospinal fluid ; ANOVA ; analysis of variance ; CFA ; complete Freund&rsquo ; s adjuvant ; CLSM ; confocal laser scanning microscope ; fEPSP ; field excitatory postsynaptic potential ; HEPES ; (4-(2-hydroxyethyl)-1-pipera
• 刊名：Neuroscience
• 出版年：2012
• 期刊代码：50_03064522
• 类别：neu
• 出版时间：2 August, 2012
• 卷：216
• 期：Complete
• 页码：133-142
• 文件大小：1226 K

摘要

Chronic systemic inflammation induces age-dependent differential phenotypic changes in microglia and astrocytes, yielding an anti-inflammatory cell phenotype in young rats and a proinflammatory cell phenotype in middle-aged rats. These observations prompted further investigation of the functional outcomes of the resultant differential microglial phenotypic changes. The present study examined the effects of age-dependent differential microglial phenotypic changes following chronic systemic inflammation on the formation of the post-tetanic potentiation (PTP) and long-term potentiation (LTP) in the hippocampus. Microglia formed a proinflammatory cell phenotype to express ED1 and interleukin-1尾 (IL-1尾) in the hippocampal CA1 region of middle-aged rats, but not in young rats following the establishment of adjuvant arthritis (AA). Furthermore, AA induced deficits in the formation of LTP in the Schaffer collateral-CA1 synapses of middle-aged rats, but not in young rats. On the other hand, the formation of PTP was impaired in both young and middle-aged AA rats. Minocycline, a known inhibitor of microglial activation, was systemically administered to middle-aged AA rats significantly restoring the mean magnitudes of both PTP and LTP. The mean expression levels of ED1 and IL-1尾 were significantly suppressed. These observations strongly suggest that chronic systemic inflammation induces deficits in the hippocampal LTP in middle-aged rats through neuroinflammation mainly induced by microglia.