Linked Life Data

3179724

Source:http://linkedlifedata.com/resource/pubmed/id/3179724

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1988-12-21
pubmed:abstractText
The effects of a calmodulin (CaM) inhibitor, which does not influence Ca2+ fluxes (calmidazolium, RO-24571), and a new potent inhibitor of protein kinase C (K-252b) on long-term potentiation (LTP) were compared in hippocampal slices. Tetanic stimulation of the stratum radiatum during perfusion of calmidazolium (50 nM) failed to induce the characteristic post-tetanic and long-term increase in the magnitude of CA1-evoked responses. During perfusion with K-252b (50 nM) post-tetanic potentiation and initial LTP is expressed normally, but thereafter declines back to baseline with a 60 min delay. By themselves, the inhibitors had no significant effect on synaptic transmission in a non-tetanized control input. Our data are in line with current evidence from several laboratories that CaM- and protein kinase C (PKC)-dependent processes are involved in LTP and support the hypothesis that CaM mediates initiation and that PKC mediates mechanisms underlying the maintenance of LTP.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
4
pubmed:volume
461
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
388-92
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Inhibitors of calmodulin and protein kinase C block different phases of hippocampal long-term potentiation.
pubmed:affiliation
Institute of Neurobiology and Brain Research, Academy of Sciences G.D.R., Magdeburg.
pubmed:publicationType
Journal Article, In Vitro