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rdf:type |
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lifeskim:mentions |
umls-concept:C0034143,
umls-concept:C0169424,
umls-concept:C0205263,
umls-concept:C0225326,
umls-concept:C0301630,
umls-concept:C0871261,
umls-concept:C1314939,
umls-concept:C1522240,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2348042,
umls-concept:C2911692
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pubmed:issue |
10
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pubmed:dateCreated |
2007-9-24
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pubmed:abstractText |
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.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amyloid beta-Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents...,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Flurbiprofen,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/NG-Nitroarginine Methyl Ester,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Nicotinic,
http://linkedlifedata.com/resource/pubmed/chemical/alpha7 nicotinic acetylcholine...,
http://linkedlifedata.com/resource/pubmed/chemical/amyloid beta-protein (1-42)
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0531-5565
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
42
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
951-62
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:17596899-Amyloid beta-Peptides,
pubmed-meshheading:17596899-Animals,
pubmed-meshheading:17596899-Anti-Inflammatory Agents, Non-Steroidal,
pubmed-meshheading:17596899-Enzyme Inhibitors,
pubmed-meshheading:17596899-Excitatory Postsynaptic Potentials,
pubmed-meshheading:17596899-Flurbiprofen,
pubmed-meshheading:17596899-Glutamic Acid,
pubmed-meshheading:17596899-Inflammation,
pubmed-meshheading:17596899-Mice,
pubmed-meshheading:17596899-Mice, Inbred C57BL,
pubmed-meshheading:17596899-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:17596899-Nitric Oxide Synthase,
pubmed-meshheading:17596899-Patch-Clamp Techniques,
pubmed-meshheading:17596899-Peptide Fragments,
pubmed-meshheading:17596899-Purkinje Cells,
pubmed-meshheading:17596899-Receptors, Nicotinic,
pubmed-meshheading:17596899-Signal Transduction,
pubmed-meshheading:17596899-Synapses,
pubmed-meshheading:17596899-Tissue Culture Techniques
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pubmed:year |
2007
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pubmed:articleTitle |
Beta-amyloid(1-42) induces a reduction in the parallel fiber responses of Purkinje cells: possible involvement of pro-inflammatory processes.
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pubmed:affiliation |
Equipe Développement et Vieillissement du Système Nerveux, UMR 7102, UPMC-CNRS, Lab DVSN, 9, Quai St Bernard, Case 14, Paris F-75005, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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