Source:http://linkedlifedata.com/resource/pubmed/id/17976923
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
8-10
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| pubmed:dateCreated |
2007-11-16
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| pubmed:abstractText |
Ample research demonstrates that pathophysiological levels of the pro-inflammatory cytokine interleukin-1 (IL-1) produces detrimental effects on memory functioning. However, recent evidence suggests that IL-1 may be required for the normal physiological regulation of hippocampal-dependent memory. To substantiate the physiological role of IL-1 in learning and memory we examined the induction of IL-1 gene expression following a learning experience, and the effects of IL-1 signaling blockade, by either genetic or pharmacological manipulations, on memory functioning. We show that IL-1 gene expression is induced in the hippocampus 24h following fear-conditioning in wild type mice, but not in two mouse strains with impaired IL-1 signaling. Moreover, we report that mice with transgenic over-expression of IL-1 receptor antagonist restricted to the CNS (IL-1raTG) display impaired hippocampal-dependent and intact hippocampal-independent memory in the water maze and fear-conditioning paradigms. We further demonstrate that continuous administration of IL-1ra via osmotic minipumps during prenatal development disrupt memory performance in adult mice, suggesting that IL-1 plays a critical role not only in the formation of hippocampal-dependent memory but also in normal hippocampal development. Finally, we tested the dual role of IL-1 in memory by intracerebroventricular (ICV) administration of different doses of IL-1beta and IL-1ra following learning, providing the first systematic evidence that the involvement of IL-1 in hippocampal-dependent memory follows an inverted U-shaped pattern, i.e., a slight increase in brain IL-1 levels can improve memory, whereas any deviation from the physiological range, either by excess elevation in IL-1 levels or by blockade of IL-1 signaling, results in impaired memory.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:issn |
0306-4530
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
32
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1106-15
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| pubmed:meshHeading |
pubmed-meshheading:17976923-Animals,
pubmed-meshheading:17976923-Animals, Newborn,
pubmed-meshheading:17976923-Avoidance Learning,
pubmed-meshheading:17976923-Conditioning (Psychology),
pubmed-meshheading:17976923-Fear,
pubmed-meshheading:17976923-Female,
pubmed-meshheading:17976923-Gene Expression Regulation,
pubmed-meshheading:17976923-Hippocampus,
pubmed-meshheading:17976923-Humans,
pubmed-meshheading:17976923-Interleukin 1 Receptor Antagonist Protein,
pubmed-meshheading:17976923-Interleukin-1,
pubmed-meshheading:17976923-Male,
pubmed-meshheading:17976923-Maze Learning,
pubmed-meshheading:17976923-Memory,
pubmed-meshheading:17976923-Memory Disorders,
pubmed-meshheading:17976923-Mice,
pubmed-meshheading:17976923-Mice, Inbred C57BL,
pubmed-meshheading:17976923-Mice, Inbred CBA,
pubmed-meshheading:17976923-Mice, Transgenic,
pubmed-meshheading:17976923-Pregnancy
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| pubmed:articleTitle |
A dual role for interleukin-1 in hippocampal-dependent memory processes.
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| pubmed:affiliation |
Department of Psychology, The Hebrew University, Jerusalem 91905, Israel.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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