pubmed-article:7910404 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7910404 | lifeskim:mentions | umls-concept:C0026845 | lld:lifeskim |
pubmed-article:7910404 | lifeskim:mentions | umls-concept:C0030685 | lld:lifeskim |
pubmed-article:7910404 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
pubmed-article:7910404 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
pubmed-article:7910404 | lifeskim:mentions | umls-concept:C0010284 | lld:lifeskim |
pubmed-article:7910404 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
pubmed-article:7910404 | lifeskim:mentions | umls-concept:C0680255 | lld:lifeskim |
pubmed-article:7910404 | lifeskim:mentions | umls-concept:C0391871 | lld:lifeskim |
pubmed-article:7910404 | lifeskim:mentions | umls-concept:C1283071 | lld:lifeskim |
pubmed-article:7910404 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
pubmed-article:7910404 | lifeskim:mentions | umls-concept:C1963578 | lld:lifeskim |
pubmed-article:7910404 | lifeskim:mentions | umls-concept:C1707723 | lld:lifeskim |
pubmed-article:7910404 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:7910404 | pubmed:dateCreated | 1994-6-16 | lld:pubmed |
pubmed-article:7910404 | pubmed:abstractText | The toxin fraction (FTX) and peptide omega-Aga-IVA from the venom of the funnel-web spider Agelenopsis aperta, as well as a synthetic analogue of FTX, specifically block the P-type voltage-dependent Ca2+ channel (VDCC). The effects of these toxins on synaptic transmission were studied in the neuromuscular synapses of the crayfish opener muscle, which has a single excitatory and a single inhibitory motoneuron. FTX selectively and reversibly blocked excitatory and inhibitory postsynaptic currents and potentials in a dose-dependent manner. FTX had no effect on (i) resting and postsynaptic membrane conductance, (ii) postsynaptic L-type VDCC, and (iii) both glutamate- and gamma-aminobutyric acid-induced postsynaptic responses. Mean amplitude and frequency of miniature postsynaptic potentials were unchanged by FTX. The postsynaptic VDCC was inhibited by nifedipine, a selective dihydropyridine antagonist of L-type VDCC, whereas synaptic transmission was unaffected. Transmission was also undisturbed by omega-conotoxin, suggesting that N-type VDCCs are not involved. The peptide omega-Aga-IVA blocked excitatory and inhibitory transmission without affecting postsynaptic VDCC. Synaptic transmission was also blocked by synthetic FTX. We conclude that presynaptic P-type VDCCs are involved in both evoked excitatory and inhibitory transmitter release in crayfish neuromuscular synapses. | lld:pubmed |
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pubmed-article:7910404 | pubmed:language | eng | lld:pubmed |
pubmed-article:7910404 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7910404 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:7910404 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7910404 | pubmed:month | May | lld:pubmed |
pubmed-article:7910404 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:7910404 | pubmed:author | pubmed-author:BuñoWW | lld:pubmed |
pubmed-article:7910404 | pubmed:author | pubmed-author:ClaracFF | lld:pubmed |
pubmed-article:7910404 | pubmed:author | pubmed-author:AraqueAA | lld:pubmed |
pubmed-article:7910404 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7910404 | pubmed:day | 10 | lld:pubmed |
pubmed-article:7910404 | pubmed:volume | 91 | lld:pubmed |
pubmed-article:7910404 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7910404 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7910404 | pubmed:pagination | 4224-8 | lld:pubmed |
pubmed-article:7910404 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:7910404 | pubmed:year | 1994 | lld:pubmed |
pubmed-article:7910404 | pubmed:articleTitle | P-type Ca2+ channels mediate excitatory and inhibitory synaptic transmitter release in crayfish muscle. | lld:pubmed |
pubmed-article:7910404 | pubmed:affiliation | Instituto Cajal Consejo Superior de Investigaciones Cientificas, Madrid, Spain. | lld:pubmed |