Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-3
|
pubmed:dateCreated |
1997-2-6
|
pubmed:abstractText |
The effects of intracellular signal transduction system inhibitors on the inward current (Iin) caused by achatin-I (Gly-D-Phe-Ala-Asp), an Achatina endogenous tetrapeptide having a D-phenylalanine residue, applied locally onto the neurone tested, were examined under voltage clamp using two identifiable Achatina giant neurone types, v-RCDN (ventral-right cerebral distinct neurone) and PON (periodically oscillating neurone). H-89 (N-[2-(p-bromocinnamylamino)-ethyl]-5-isoquinolinesulfonamide) (adenosine-3',5'-cyclic monophosphate (cyclic AMP)-dependent protein kinase inhibitor) markedly suppressed the achatin-I-induced Iin on PON, whereas this drug was ineffective on the Iin of v-RCDN. Dose (pressure duration)-response study of achatin-I on PON in a physiological solution and in the presence of H-89, and Lineweaver-Burk plot of these data, indicated that H-89 inhibited the Iin in a noncompetitive manner. KT5823 (N-methyl-(8R*,9S*,11S*)-(-)-9-methoxy-9-methoxycarbonyl-8-methyl-2,3,9, 10-tetrahydro-8,11-epoxy-1H,8H,11H-2, 7b,11a-triazadibenzo[a,g]cycloocta[c,d,e]-trinden-1-on e) (guanosine-3',5'-cyclic monophosphate (cyclic GMP)-dependent protein kinase inhibitor) suppressed the achatin-I-induced Iin of v-RCDN in mainly noncompetitive and partly uncompetitive manners, but this drug had no effect on the Iin of PON. W-7 (N-(6-aminohexyl)-5-chloro-1-naphthalene-sulfonamide) (calmodulin inhibitor) suppressed noncompetitively the Iin of PON, but this drug had no effect on the Iin of v-RCDN. IBMX (3-isobutyl-1-methylxanthine) (cyclic nucleotide phosphodiesterase inhibitor) enhanced the achatin-I-induced Iin of v-RCDN, but this drug was ineffective on the Iin of PON. However, IBMX might have effects on the achatin-I receptor sites on v-RCDN. These findings suggest multiple intracellular signal transduction pathways mediating the achatin-I-induced Iin: the Iin of PON is via cyclic AMP-dependent and probably Ca2+/calmodulin-dependent protein kinases, and that of v-RCDN via cyclic GMP-dependent protein kinase. Other signal transduction system inhibitors including calphostin C (2-[12-[2-(benzyloxy)-propyl]-3, 10-dihydro-4,9-dihydroxy-2,6,7,11-tetramethoxy-3,10-dioxo-1-per yleny]-1 -methylethyl carbonic acid 4-hydroxyphenyl ester) (protein kinase C inhibitor) did not significantly affect the Iin of both v-RCDN and PON.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1-Methyl-3-isobutylxanthine,
http://linkedlifedata.com/resource/pubmed/chemical/Alkaloids,
http://linkedlifedata.com/resource/pubmed/chemical/Carbazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Indoles,
http://linkedlifedata.com/resource/pubmed/chemical/Isoquinolines,
http://linkedlifedata.com/resource/pubmed/chemical/KT 5823,
http://linkedlifedata.com/resource/pubmed/chemical/N-(2-(4-bromocinnamylamino)ethyl)-5-...,
http://linkedlifedata.com/resource/pubmed/chemical/Naphthalenes,
http://linkedlifedata.com/resource/pubmed/chemical/Neuropeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Neurotransmitter Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphodiesterase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfonamides,
http://linkedlifedata.com/resource/pubmed/chemical/Vasodilator Agents,
http://linkedlifedata.com/resource/pubmed/chemical/W 7,
http://linkedlifedata.com/resource/pubmed/chemical/achatin I,
http://linkedlifedata.com/resource/pubmed/chemical/calphostin C
|
pubmed:status |
MEDLINE
|
pubmed:month |
Apr
|
pubmed:issn |
0014-2999
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
29
|
pubmed:volume |
302
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
129-39
|
pubmed:dateRevised |
2010-11-18
|
pubmed:meshHeading |
pubmed-meshheading:8791001-1-Methyl-3-isobutylxanthine,
pubmed-meshheading:8791001-Alkaloids,
pubmed-meshheading:8791001-Analysis of Variance,
pubmed-meshheading:8791001-Animals,
pubmed-meshheading:8791001-Carbazoles,
pubmed-meshheading:8791001-Dose-Response Relationship, Drug,
pubmed-meshheading:8791001-Indoles,
pubmed-meshheading:8791001-Isoquinolines,
pubmed-meshheading:8791001-Naphthalenes,
pubmed-meshheading:8791001-Neurons,
pubmed-meshheading:8791001-Neuropeptides,
pubmed-meshheading:8791001-Neurotransmitter Agents,
pubmed-meshheading:8791001-Patch-Clamp Techniques,
pubmed-meshheading:8791001-Phosphodiesterase Inhibitors,
pubmed-meshheading:8791001-Protein Kinase C,
pubmed-meshheading:8791001-Protein Kinase Inhibitors,
pubmed-meshheading:8791001-Signal Transduction,
pubmed-meshheading:8791001-Snails,
pubmed-meshheading:8791001-Sulfonamides,
pubmed-meshheading:8791001-Vasodilator Agents
|
pubmed:year |
1996
|
pubmed:articleTitle |
Multiple intracellular signal transduction pathways mediating inward current produced by the neuropeptide, achatin-I.
|
pubmed:affiliation |
Department of Physiology, Gifu University School of Medicine, Japan.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|