| pubmed-article:2161529 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2161529 | lifeskim:mentions | umls-concept:C1273518 | lld:lifeskim |
| pubmed-article:2161529 | lifeskim:mentions | umls-concept:C0019564 | lld:lifeskim |
| pubmed-article:2161529 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:2161529 | lifeskim:mentions | umls-concept:C0206249 | lld:lifeskim |
| pubmed-article:2161529 | lifeskim:mentions | umls-concept:C1150572 | lld:lifeskim |
| pubmed-article:2161529 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:2161529 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:2161529 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:2161529 | pubmed:dateCreated | 1990-7-12 | lld:pubmed |
| pubmed-article:2161529 | pubmed:abstractText | Long-term potentiation (LTP) in hippocampus has been proposed to result from a tonic activation of protein kinase C. This hypothesis predicts that stimulation of the kinase would produce a smaller change in response size on potentiated versus control pathways and, conversely, that inhibition of the kinase would reduce potentiated inputs to a greater degree than control responses. We tested these predictions using phorbol esters to activate and using the antagonist H-7 to inhibit protein kinase C; we found that the actions of these drugs on synaptic transmission were not affected by prior induction of LTP. Both compounds, however, significantly decreased the contribution of N-methyl-D-aspartate receptors to synaptic potentials, a result that accounts for the suppressive effects of these compounds on LTP formation. Thus protein kinase C is probably not involved in the expression of LTP but may play a role in the receptor-mediated events participating in its induction. | lld:pubmed |
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| pubmed-article:2161529 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2161529 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2161529 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2161529 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2161529 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:2161529 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:2161529 | pubmed:author | pubmed-author:DunantYY | lld:pubmed |
| pubmed-article:2161529 | pubmed:author | pubmed-author:MullerDD | lld:pubmed |
| pubmed-article:2161529 | pubmed:author | pubmed-author:LynchGG | lld:pubmed |
| pubmed-article:2161529 | pubmed:author | pubmed-author:BuchsP APA | lld:pubmed |
| pubmed-article:2161529 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2161529 | pubmed:volume | 87 | lld:pubmed |
| pubmed-article:2161529 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2161529 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2161529 | pubmed:pagination | 4073-7 | lld:pubmed |
| pubmed-article:2161529 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:2161529 | pubmed:meshHeading | pubmed-meshheading:2161529-... | lld:pubmed |
| pubmed-article:2161529 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:2161529 | pubmed:articleTitle | Protein kinase C activity is not responsible for the expression of long-term potentiation in hippocampus. | lld:pubmed |
| pubmed-article:2161529 | pubmed:affiliation | Department of Pharmacology, Centre Medical Universitaire, Geneva, Switzerland. | lld:pubmed |
| pubmed-article:2161529 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2161529 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:2161529 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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