pubmed-article:8570023 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8570023 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
pubmed-article:8570023 | lifeskim:mentions | umls-concept:C0020663 | lld:lifeskim |
pubmed-article:8570023 | lifeskim:mentions | umls-concept:C0243046 | lld:lifeskim |
pubmed-article:8570023 | lifeskim:mentions | umls-concept:C0205409 | lld:lifeskim |
pubmed-article:8570023 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:8570023 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
pubmed-article:8570023 | lifeskim:mentions | umls-concept:C0057676 | lld:lifeskim |
pubmed-article:8570023 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
pubmed-article:8570023 | lifeskim:mentions | umls-concept:C0301625 | lld:lifeskim |
pubmed-article:8570023 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:8570023 | pubmed:dateCreated | 1996-3-4 | lld:pubmed |
pubmed-article:8570023 | pubmed:abstractText | Ionic currents induced by excitatory amino acids were investigated for freshly isolated murine hypothalamic neurons with whole cell recording techniques. L-glutamate or N-methyl-D-aspartate (NMDA), in combination with glycine, resulted in a rapidly rising current which decayed in the continued presence of agonist. In contrast, kainate currents did not decay. While quisqualate-induced current maintained a steady amplitude in the continued presence of agonist, a rapid decay phase appeared at holding potentials negative to -50 mV. Co-application of 2,3-butanedione monoxime (BDM) reversibly inhibited the currents due to each agonist. Detailed study of BDM suppression of kainate-induced current revealed two components. A component with a rapid onset did not involve phosphatase action since 500 microM ATP-gamma-S or a protein kinase inhibitor (H-7, 200 microM) did not alter current suppression or recovery after BDM. Thus, the probable mechanism for this component of BDM's effect is direct block of the kainate-activated ion channel. However, preincubating neurons with 30 mM BDM reduced their subsequent response to kainate alone. This persistent effect of BDM was not seen for neurons dialyzed with a solution containing ATP-gamma-S during conventional whole cell recording. Furthermore, exposure to H-7 prevented recovery of the kainate response suppressed by preincubation in BDM. These findings suggest that BDM causes sustained suppression of the kainate response of hypothalamic neurons via a "chemical phosphatase" action. | lld:pubmed |
pubmed-article:8570023 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8570023 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8570023 | pubmed:language | eng | lld:pubmed |
pubmed-article:8570023 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8570023 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:8570023 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8570023 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8570023 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8570023 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8570023 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8570023 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8570023 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8570023 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8570023 | pubmed:month | Oct | lld:pubmed |
pubmed-article:8570023 | pubmed:issn | 0028-3908 | lld:pubmed |
pubmed-article:8570023 | pubmed:author | pubmed-author:McArdleJ JJJ | lld:pubmed |
pubmed-article:8570023 | pubmed:author | pubmed-author:YeJ HJH | lld:pubmed |
pubmed-article:8570023 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8570023 | pubmed:volume | 34 | lld:pubmed |
pubmed-article:8570023 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8570023 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8570023 | pubmed:pagination | 1259-72 | lld:pubmed |
pubmed-article:8570023 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
pubmed-article:8570023 | pubmed:meshHeading | pubmed-meshheading:8570023-... | lld:pubmed |
pubmed-article:8570023 | pubmed:meshHeading | pubmed-meshheading:8570023-... | lld:pubmed |
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pubmed-article:8570023 | pubmed:meshHeading | pubmed-meshheading:8570023-... | lld:pubmed |
pubmed-article:8570023 | pubmed:meshHeading | pubmed-meshheading:8570023-... | lld:pubmed |
pubmed-article:8570023 | pubmed:meshHeading | pubmed-meshheading:8570023-... | lld:pubmed |
pubmed-article:8570023 | pubmed:meshHeading | pubmed-meshheading:8570023-... | lld:pubmed |
pubmed-article:8570023 | pubmed:year | 1995 | lld:pubmed |
pubmed-article:8570023 | pubmed:articleTitle | Excitatory amino acid induced currents of isolated murine hypothalamic neurons and their suppression by 2,3-butanedione monoxime. | lld:pubmed |
pubmed-article:8570023 | pubmed:affiliation | Department of Anesthesiology, New Jersey Medical School (UMDNJ), Newark 07103-2714, USA. | lld:pubmed |
pubmed-article:8570023 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8570023 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8570023 | lld:pubmed |