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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0001613,
umls-concept:C0007776,
umls-concept:C0010453,
umls-concept:C0016904,
umls-concept:C0022655,
umls-concept:C0030685,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0205225,
umls-concept:C0206529,
umls-concept:C0391871,
umls-concept:C0439064,
umls-concept:C0680255,
umls-concept:C0851285,
umls-concept:C1283071,
umls-concept:C1704259,
umls-concept:C1705987,
umls-concept:C1963578
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pubmed:issue |
1-2
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pubmed:dateCreated |
1998-5-14
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pubmed:abstractText |
In rat cortical primary cultures, group II- and III-metabotropic glutamate receptor-selective agonists concentration-dependently reduced KCl-induced [3H]GABA release, with IC50 values of 11 nM for LY354740, 80 nM for L(+)-2-amino-4-phosphonobutyric acid (L-AP4), 180 nM for DCG-IV, and 330 nM for L-SOP. The group II antagonists, LY341495 and EGLU, reversed the effect of LY354740, and the group III antagonist MTPG reversed the effect of L-AP4. In the presence of omega-conotoxin GVIA, LY354740 inhibited the remaining [3H]GABA release, whereas L-AP4 was inactive. In contrast, in the presence of nifedipine, L-AP4 inhibited the remaining [3H]GABA release, but LY354740 was no longer active. The PKA inhibitor, H89, blocked the effects of both L-AP4 and LY354740, whereas the PKC inhibitor Ro 31-8220 blocked only the effect of LY354740. Both Ro 31-8220 and H89 reduced the [3H]GABA release to 60% of control. In whole-cell, voltage-clamp experiments, LY354740 and L-AP4 inhibited voltage-gated calcium channel currents with IC50 values of 28 nM and 22 microM, respectively. The results suggest that, in these cells, KCl-induced [3H]GABA release is modulated by two different mechanisms, one involving group II receptors and a direct control of the Ca2+ channel activity, and the other mediated by group III receptors and possibly involving a regulation located downstream of the Ca2+ channel activation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Metabotropic Glutamate,
http://linkedlifedata.com/resource/pubmed/chemical/Tritium,
http://linkedlifedata.com/resource/pubmed/chemical/gamma-Aminobutyric Acid
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0006-8993
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
26
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pubmed:volume |
782
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
91-104
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pubmed:dateRevised |
2003-11-14
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pubmed:meshHeading |
pubmed-meshheading:9519253-Animals,
pubmed-meshheading:9519253-Blotting, Western,
pubmed-meshheading:9519253-Cells, Cultured,
pubmed-meshheading:9519253-Cerebral Cortex,
pubmed-meshheading:9519253-Cyclic AMP,
pubmed-meshheading:9519253-In Situ Hybridization,
pubmed-meshheading:9519253-Patch-Clamp Techniques,
pubmed-meshheading:9519253-Potassium Chloride,
pubmed-meshheading:9519253-Rats,
pubmed-meshheading:9519253-Rats, Inbred Strains,
pubmed-meshheading:9519253-Receptors, Metabotropic Glutamate,
pubmed-meshheading:9519253-Tritium,
pubmed-meshheading:9519253-gamma-Aminobutyric Acid
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pubmed:year |
1998
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pubmed:articleTitle |
Multiple pathways for regulation of the KCl-induced [3H]-GABA release by metabotropic glutamate receptors, in primary rat cortical cultures.
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pubmed:affiliation |
Pharma Division Preclinical CNS Research, F. Hoffmann-La Roche, Basel, Switzerland. herve.Schaffhauser@roche.com
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pubmed:publicationType |
Journal Article
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