rdf:type |
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lifeskim:mentions |
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pubmed:issue |
24
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pubmed:dateCreated |
1995-12-28
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pubmed:abstractText |
Ca(2+)-sensitive kinases are thought to play a role in long-term potentiation (LTP). To test the involvement of Ca2+/calmodulin-dependent kinase II (CaM-K II), truncated, constitutively active form of this kinase was directly injected into CA1 hippocampal pyramidal cells. Inclusion of CaM-K II in the recording pipette resulted in a gradual increase in the size of excitatory postsynaptic currents (EPSCs). No change in evoked responses occurred when the pipette contained heat-inactivated kinase. The effects of CaM-K II mimicked several features of LTP in that it caused a decreased incidence of synaptic failures, an increase in the size of spontaneous EPSCs, and an increase in the amplitude of responses to iontophoretically applied alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate. To determine whether the CaM-K II-induced enhancement and LTP share a common mechanism, occlusion experiments were carried out. The enhancing action of CaM-K II was greatly diminished by prior induction of LTP. In addition, following the increase in synaptic strength by CaM-K II, tetanic stimulation failed to evoke LTP. These findings indicate that CaM-K II alone is sufficient to augment synaptic strength and that this enhancement shares the same underlying mechanism as the enhancement observed with LTP.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/7479960-1317014,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7479960-1334418,
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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:month |
Nov
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pubmed:issn |
0027-8424
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
21
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pubmed:volume |
92
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
11175-9
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:7479960-Animals,
pubmed-meshheading:7479960-Calcium,
pubmed-meshheading:7479960-Calcium-Calmodulin-Dependent Protein Kinase Type 2,
pubmed-meshheading:7479960-Calcium-Calmodulin-Dependent Protein Kinases,
pubmed-meshheading:7479960-Enzyme Activation,
pubmed-meshheading:7479960-Guinea Pigs,
pubmed-meshheading:7479960-Hippocampus,
pubmed-meshheading:7479960-Long-Term Potentiation,
pubmed-meshheading:7479960-Microinjections,
pubmed-meshheading:7479960-Receptors, AMPA,
pubmed-meshheading:7479960-Synaptic Transmission
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pubmed:year |
1995
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pubmed:articleTitle |
Calcium/calmodulin-dependent kinase II and long-term potentiation enhance synaptic transmission by the same mechanism.
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pubmed:affiliation |
Department of Cellular and Molecular Pharmacology, University of California, San Francisco 94143-0450, USA.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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