| pubmed-article:8269509 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8269509 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:8269509 | lifeskim:mentions | umls-concept:C0019564 | lld:lifeskim |
| pubmed-article:8269509 | lifeskim:mentions | umls-concept:C0033634 | lld:lifeskim |
| pubmed-article:8269509 | lifeskim:mentions | umls-concept:C0206249 | lld:lifeskim |
| pubmed-article:8269509 | lifeskim:mentions | umls-concept:C0205349 | lld:lifeskim |
| pubmed-article:8269509 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:8269509 | pubmed:dateCreated | 1994-1-31 | lld:pubmed |
| pubmed-article:8269509 | pubmed:abstractText | Calcium-phospholipid-dependent protein kinase (PKC) has long been suggested to play an important role in modulating synaptic efficacy. We have created a strain of mice that lacks the gamma subtype of PKC to evaluate the significance of this brain-specific PKC isozyme in synaptic plasticity. Mutant mice are viable, develop normally, and have synaptic transmission that is indistinguishable from wild-type mice. Long-term potentiation (LTP), however, is greatly diminished in mutant animals, while two other forms of synaptic plasticity, long-term depression and paired-pulse facilitation, are normal. Surprisingly, when tetanus to evoke LTP was preceded by a low frequency stimulation, mutant animals displayed apparently normal LTP. We propose that PKC gamma is not part of the molecular machinery that produces LTP but is a key regulatory component. | lld:pubmed |
| pubmed-article:8269509 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8269509 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8269509 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8269509 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8269509 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8269509 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8269509 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:8269509 | pubmed:issn | 0092-8674 | lld:pubmed |
| pubmed-article:8269509 | pubmed:author | pubmed-author:AbeliovichAA | lld:pubmed |
| pubmed-article:8269509 | pubmed:author | pubmed-author:ChenCC | lld:pubmed |
| pubmed-article:8269509 | pubmed:author | pubmed-author:StevensC FCF | lld:pubmed |
| pubmed-article:8269509 | pubmed:author | pubmed-author:TonegawaSS | lld:pubmed |
| pubmed-article:8269509 | pubmed:author | pubmed-author:SilvaA JAJ | lld:pubmed |
| pubmed-article:8269509 | pubmed:author | pubmed-author:GodaYY | lld:pubmed |
| pubmed-article:8269509 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8269509 | pubmed:day | 31 | lld:pubmed |
| pubmed-article:8269509 | pubmed:volume | 75 | lld:pubmed |
| pubmed-article:8269509 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8269509 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8269509 | pubmed:pagination | 1253-62 | lld:pubmed |
| pubmed-article:8269509 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:8269509 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8269509 | pubmed:articleTitle | Modified hippocampal long-term potentiation in PKC gamma-mutant mice. | lld:pubmed |
| pubmed-article:8269509 | pubmed:affiliation | Howard Hughes Medical Institute, Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139. | lld:pubmed |
| pubmed-article:8269509 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8269509 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:8269509 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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