Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
|
| pubmed:dateCreated |
1994-11-1
|
| pubmed:abstractText |
We found in cultured glioma (C6BU-1) cells that excitatory amino acids (EAAs) such as glutamate, N-methyl-D-aspartate (NMDA), aspartate, and metabotropic glutamate receptor agonist trans-(+/-)-1-amino-1,3-cyclopentanedicarboxylate caused an increase in the inositol 1,4,5-trisphosphate formation and the intracellular Ca2+ concentration ([Ca2+]i) in the absence of extracellular Mg2+ and Ca2+. Pertussis toxin treatment abolished this glutamate-induced [Ca2+]i increase. Various antagonists against NMDA receptor-ion channel complex, such as Mg2+, D-2-amino-5-phosphonovalerate (D-APV), HA-966, and MK-801, also inhibited the increase in [Ca2+]i induced by glutamate. These results indicate that these metabotropic EAA receptors coupled to pertussis toxin-susceptible GTP-binding protein and phospholipase C system in C6BU-1 glioma cells have the pharmacological properties of NMDA receptor-ion channel complexes. We also found that in the presence of Mg2+ these metabotropic receptors resemble the NMDA receptor-ion channel complex interacted with 5-hydroxytryptamine2 (5-HT2) receptor signaling. EAAs inhibited 5-HT2 receptor-mediated intracellular Ca2+ mobilization and inositol 1,4,5-trisphosphate formation in a concentration-dependent manner. The inhibitory effect of glutamate was reversed by various NMDA receptor antagonists (D-APV, MK-801, phencyclidine, and HA-966), but L-APV failed to block the inhibitory effect of glutamate. The same result was observed in the absence of extracellular Ca2+. In addition, this inhibitory effect on 5-HT2 receptor-mediated signal transduction was abolished by treatment of C6BU-1 cells with pertussis toxin, whereas 5-HT2 receptor-mediated [Ca2+]i increase was not abolished by pertussis toxin treatment. We can, therefore, conclude that the inhibitory effect of glutamate is not a result of the influx of Ca2+ through the ion channel and that it operates via metabotropic glutamate receptors, having NMDA receptor-ion channel complex-like properties and being coupled with pertussis toxin-sensitive GTP-binding protein and phospholipase C.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1-amino-1,3-dicarboxycyclopentane,
http://linkedlifedata.com/resource/pubmed/chemical/2-Amino-5-phosphonovalerate,
http://linkedlifedata.com/resource/pubmed/chemical/Aspartic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Cycloleucine,
http://linkedlifedata.com/resource/pubmed/chemical/Dizocilpine Maleate,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/HA 966,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Kainic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Magnesium Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/N-Methylaspartate,
http://linkedlifedata.com/resource/pubmed/chemical/Neurotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrrolidinones,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Metabotropic Glutamate,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, N-Methyl-D-Aspartate,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Serotonin
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Oct
|
| pubmed:issn |
0022-3042
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
63
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1346-53
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:7523590-2-Amino-5-phosphonovalerate,
pubmed-meshheading:7523590-Animals,
pubmed-meshheading:7523590-Aspartic Acid,
pubmed-meshheading:7523590-Calcium,
pubmed-meshheading:7523590-Cell Line,
pubmed-meshheading:7523590-Cycloleucine,
pubmed-meshheading:7523590-Dizocilpine Maleate,
pubmed-meshheading:7523590-Glioma,
pubmed-meshheading:7523590-Glutamic Acid,
pubmed-meshheading:7523590-Inositol 1,4,5-Trisphosphate,
pubmed-meshheading:7523590-Ion Channels,
pubmed-meshheading:7523590-Kainic Acid,
pubmed-meshheading:7523590-Kinetics,
pubmed-meshheading:7523590-Magnesium Chloride,
pubmed-meshheading:7523590-N-Methylaspartate,
pubmed-meshheading:7523590-Neurotoxins,
pubmed-meshheading:7523590-Pyrrolidinones,
pubmed-meshheading:7523590-Rats,
pubmed-meshheading:7523590-Receptors, Metabotropic Glutamate,
pubmed-meshheading:7523590-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:7523590-Receptors, Serotonin,
pubmed-meshheading:7523590-Signal Transduction,
pubmed-meshheading:7523590-Tumor Cells, Cultured
|
| pubmed:year |
1994
|
| pubmed:articleTitle |
Metabotropic glutamate receptor in C6BU-1 glioma cell has NMDA receptor-ion channel complex-like properties and interacts with serotonin2 receptor-stimulated signal transduction.
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| pubmed:affiliation |
Department of Mental Disorder Research, National Institute of Neuroscience, Tokyo, Japan.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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