Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1990-2-6
pubmed:abstractText
We used rabbit hippocampus slices preincubated with [3H]noradrenaline (NA) and applied short pulses of 3,4-diaminopyridine (3,4-DAP) during superfusion to investigate the mechanism underlying the 3H overflow evoked by 3,4-DAP and the effects of the protein kinase C (PKC) activator, 4 beta-phorbol 12,13-dibutyrate (PDB), in this model. The 3H overflow evoked by 200 microM 3,4-DAP (about 4-5% of tissue-tritium) was largely Ca2+-dependent, tetrodotoxin-sensitive and markedly reduced by clonidine, but it was enhanced by yohimbine. We also demonstrated that the response could be inhibited via presynaptic adenosine (A1-) and opioid (kappa-) receptors. PDB (1 microM) markedly increased the 3,4-DAP-evoked 3H overflow, its effect being almost unchanged following activation of presynaptic alpha 2-, A1- or kappa-receptors. Inhibitors of PKC (polymyxin B, staurosporine) almost abolished the 3,4-DAP-evoked 3H overflow and antagonized the effects of PDB. It is concluded that application of 3,4-DAP (200 microM for 2 min) to brain slices leads to depolarization of the neuronal membrane, Na+ current-carried action potentials, Ca2+ influx and the exocytotic release of NA, which in many aspects resembles the release evoked by electrical field stimulation. The findings with phorbol ester further support the involvement of PKC in transmitter release. Activation of PKC apparently does not directly interfere with signal transduction mechanisms of presynaptic inhibitory receptors on noradrenergic nerve terminals.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
4
pubmed:volume
169
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
115-23
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
3,4-Diaminopyridine-induced noradrenaline release from CNS tissue as a model for action potential-evoked transmitter release: effects of phorbol ester.
pubmed:affiliation
Institut für Pharmakologie und Toxikologie, Universität Freiburg, F.R.G.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't