Linked Life Data

21571042

Source:http://linkedlifedata.com/resource/pubmed/id/21571042

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2011-6-6
pubmed:abstractText
Sepsis induces multiple organ dysfunction syndrome including septic encephalopathy (SE), which results in cognitive impairment. However, an effective treatment for SE remains unknown. We determined the role of interleukin-1? (IL-1?) in long-term potentiation (LTP) deficiency after SE. At first, endotoxin level in the blood was increased at 24 h after cecum ligation and puncture (CLP) (i.e. SE model). Second, the expression of IL-1? and its receptor in the hippocampus was determined by immunohistochemistry and immunoblotting. The number of Iba1-positive cells and their expression of IL-1? were enhanced by CLP with disruption of the blood brain barrier. Also, Iba1, IL-1?, and occludin protein expressions were consistent with immunohistochemical results. Third, we used an electrophysiological technique and observed the LTP deficiency, a hallmark of learning and memory, in the slices of hippocampus after CLP. Since type 1 interleukin-1 receptors (IL-1R1s) on neuronal cells were increased in the hippocampus, we utilized IL-1R1 antagonist. Pre-incubation with IL-1R1 antagonist for 30 min before recording of field excitatory post-synaptic potentials (fEPSPs) in the hippocampus canceled LTP deficiency after CLP. These results suggest the novel importance of IL-1? in synaptic plasticity deficiency associated with sepsis-induced brain inflammation. In a mouse model of SE, IL-1R1 inhibition is important in protecting synaptic function of the hippocampus after induction of SE.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1873-7544
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
28
pubmed:volume
187
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
63-9
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Interleukin-1? causes long-term potentiation deficiency in a mouse model of septic encephalopathy.
pubmed:affiliation
Department of Trauma and Acute Critical Care Center, Osaka University Hospital, Osaka, Japan. yimamura-ns@umin.net
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't