pubmed-article:12595694 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12595694 | lifeskim:mentions | umls-concept:C2337074 | lld:lifeskim |
pubmed-article:12595694 | lifeskim:mentions | umls-concept:C0682698 | lld:lifeskim |
pubmed-article:12595694 | lifeskim:mentions | umls-concept:C0020429 | lld:lifeskim |
pubmed-article:12595694 | lifeskim:mentions | umls-concept:C0678558 | lld:lifeskim |
pubmed-article:12595694 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
pubmed-article:12595694 | pubmed:issue | 5610 | lld:pubmed |
pubmed-article:12595694 | pubmed:dateCreated | 2003-2-21 | lld:pubmed |
pubmed-article:12595694 | pubmed:abstractText | Inflammation, trauma, or nerve injury may cause enduring hyperalgesia, an enhanced sensitivity to painful stimuli. Neurons in lamina I of the spinal dorsal horn that express the neurokinin 1 receptor for substance P mediate this abnormal pain sensitivity by an unknown cellular mechanism. We report that in these, but not in other nociceptive lamina I cells, neurokinin 1 receptor-activated signal transduction pathways and activation of low-threshold (T-type) voltage-gated calcium channels synergistically facilitate activity- and calcium-dependent long-term potentiation at synapses from nociceptive nerve fibers. Thereby, memory traces of painful events are retained. | lld:pubmed |
pubmed-article:12595694 | pubmed:language | eng | lld:pubmed |
pubmed-article:12595694 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12595694 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:12595694 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12595694 | pubmed:month | Feb | lld:pubmed |
pubmed-article:12595694 | pubmed:issn | 1095-9203 | lld:pubmed |
pubmed-article:12595694 | pubmed:author | pubmed-author:IkedaHiroshiH | lld:pubmed |
pubmed-article:12595694 | pubmed:author | pubmed-author:RuscheweyhRut... | lld:pubmed |
pubmed-article:12595694 | pubmed:author | pubmed-author:HeinkeBernhar... | lld:pubmed |
pubmed-article:12595694 | pubmed:author | pubmed-author:SandkühlerJur... | lld:pubmed |
pubmed-article:12595694 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:12595694 | pubmed:day | 21 | lld:pubmed |
pubmed-article:12595694 | pubmed:volume | 299 | lld:pubmed |
pubmed-article:12595694 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12595694 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12595694 | pubmed:pagination | 1237-40 | lld:pubmed |
pubmed-article:12595694 | pubmed:dateRevised | 2007-3-19 | lld:pubmed |
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pubmed-article:12595694 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12595694 | pubmed:articleTitle | Synaptic plasticity in spinal lamina I projection neurons that mediate hyperalgesia. | lld:pubmed |
pubmed-article:12595694 | pubmed:affiliation | Institute of Physiology and Pathophysiology, Heidelberg University, D-69120 Heidelberg, Germany. | lld:pubmed |
pubmed-article:12595694 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12595694 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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