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• W2061285253 abstract "In Alzheimer's disease there is an increased production of the toxic beta-amyloid peptides (Abeta), especially the longer forms such as Abeta(1-42). Using the patch-clamp technique we have studied the contribution of early pro-inflammatory processes to the acute effects of 1 microM Abeta(1-42) on the parallel fiber EPSC (PF-EPSC) of Purkinje cells in cerebellar slices. Abeta(1-42) induces a decrease in the PF-EPSC amplitude. This decrease is accompanied by a decrease in the frequency and amplitude of the miniature EPSCs, suggesting that Abeta acts at both pre- and post-synaptic sites. In the presence of L-NAME, a nitric oxide synthase inhibitor, the effects of Abeta were partially blocked. The frequency of mEPSCs was unchanged while Abeta still reduced the mEPSCs amplitude. The anti-inflammatory agent flurbiprofen blocked the depressant action of Abeta on the mEPSCs amplitude but not its effect on mEPSCs frequency. Both a p38 inhibitor (SB203580) and a JNK inhibitor (SP600125) reverse the effects of Abeta as an increase in the mEPSCs frequency and amplitude was observed. This study provides evidence that the Abeta-induced depression of the PF-EPSCs was mediated via an activation of JNK and p38 and by the action of NO and raises the possibility of the involvement of an early pro-inflammatory process." @default.
• W2061285253 created "2016-06-24" @default.
• W2061285253 creator A5010262899 @default.
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• W2061285253 creator A5064197824 @default.
• W2061285253 creator A5089837015 @default.
• W2061285253 date "2007-10-01" @default.
• W2061285253 modified "2023-10-18" @default.
• W2061285253 title "β-Amyloid(1–42) induces a reduction in the parallel fiber responses of Purkinje cells: Possible involvement of pro-inflammatory processes" @default.
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• W2061285253 doi "https://doi.org/10.1016/j.exger.2007.05.007" @default.
• W2061285253 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17596899" @default.
• W2061285253 hasPublicationYear "2007" @default.
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