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| pubmed-article:18947392 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:18947392 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:18947392 | lifeskim:mentions | umls-concept:C0019564 | lld:lifeskim |
| pubmed-article:18947392 | lifeskim:mentions | umls-concept:C0001443 | lld:lifeskim |
| pubmed-article:18947392 | lifeskim:mentions | umls-concept:C1120843 | lld:lifeskim |
| pubmed-article:18947392 | lifeskim:mentions | umls-concept:C1413038 | lld:lifeskim |
| pubmed-article:18947392 | lifeskim:mentions | umls-concept:C0205146 | lld:lifeskim |
| pubmed-article:18947392 | lifeskim:mentions | umls-concept:C1136141 | lld:lifeskim |
| pubmed-article:18947392 | pubmed:dateCreated | 2008-11-5 | lld:pubmed |
| pubmed-article:18947392 | pubmed:abstractText | Although long-term potentiation (LTP) of synaptic strength is very persistent, current studies have provided evidence that various manipulations or pharmacological treatment when applied shortly after LTP induction can reverse it. This kind of reversal of synaptic strength is termed as depotentiation and may have a function to increase the flexibility and storage capacity of neuronal networks. Our previous studies have demonstrated that an increase in extracellular levels of adenosine and subsequent activation of adenosine A? receptors are important for the induction of depotentiation; however, the signaling downstream of adenosine A? receptors to mediate depotentiation induction remains elusive. | lld:pubmed |
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| pubmed-article:18947392 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18947392 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18947392 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18947392 | pubmed:issn | 1756-6606 | lld:pubmed |
| pubmed-article:18947392 | pubmed:author | pubmed-author:HuangChiung-C... | lld:pubmed |
| pubmed-article:18947392 | pubmed:author | pubmed-author:HsuKuei-SenKS | lld:pubmed |
| pubmed-article:18947392 | pubmed:author | pubmed-author:LiangYing-Chi... | lld:pubmed |
| pubmed-article:18947392 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18947392 | pubmed:volume | 1 | lld:pubmed |
| pubmed-article:18947392 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18947392 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18947392 | pubmed:pagination | 13 | lld:pubmed |
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| pubmed-article:18947392 | pubmed:meshHeading | pubmed-meshheading:18947392... | lld:pubmed |
| pubmed-article:18947392 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18947392 | pubmed:articleTitle | A role of p38 mitogen-activated protein kinase in adenosine A? receptor-mediated synaptic depotentiation in area CA1 of the rat hippocampus. | lld:pubmed |
| pubmed-article:18947392 | pubmed:affiliation | Department of Pharmacology, National Cheng Kung University, Tainan City, Taiwan. alice217@ms35.url.com.tw | lld:pubmed |
| pubmed-article:18947392 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18947392 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:18947392 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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