| pubmed-article:11599006 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11599006 | lifeskim:mentions | umls-concept:C0010453 | lld:lifeskim |
| pubmed-article:11599006 | lifeskim:mentions | umls-concept:C0682702 | lld:lifeskim |
| pubmed-article:11599006 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
| pubmed-article:11599006 | lifeskim:mentions | umls-concept:C0107103 | lld:lifeskim |
| pubmed-article:11599006 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:11599006 | lifeskim:mentions | umls-concept:C0220839 | lld:lifeskim |
| pubmed-article:11599006 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
| pubmed-article:11599006 | lifeskim:mentions | umls-concept:C0030685 | lld:lifeskim |
| pubmed-article:11599006 | lifeskim:mentions | umls-concept:C0680255 | lld:lifeskim |
| pubmed-article:11599006 | lifeskim:mentions | umls-concept:C0391871 | lld:lifeskim |
| pubmed-article:11599006 | lifeskim:mentions | umls-concept:C1283071 | lld:lifeskim |
| pubmed-article:11599006 | lifeskim:mentions | umls-concept:C1963578 | lld:lifeskim |
| pubmed-article:11599006 | lifeskim:mentions | umls-concept:C0439831 | lld:lifeskim |
| pubmed-article:11599006 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:11599006 | pubmed:dateCreated | 2001-10-12 | lld:pubmed |
| pubmed-article:11599006 | pubmed:abstractText | We reported previously that BDNF induced glutamate release was dependent on intracellular Ca(2+) but not extracellular Ca(2+) in cerebellar neurons (Numakawa et al., 1999). It was revealed that the release was through a non-exocytotic pathway (Takei et al., 1998; Numakawa et al., 1999). In the present study, we monitored the dynamics of intracellular Ca(2+) and Na(+) in cerebellar neurons, and investigated the possibility of reverse transport of glutamate mediated by BDNF. As reported, BDNF increased the intracellular Ca(2+) level. We found that the Ca(2+) increase induced by BDNF was completely blocked by xestospongin C, an IP(3) receptor antagonist, and U-73122, a PLC-gamma inhibitor. Xestospongin C and U-73122 also blocked the BDNF-dependent glutamate release, suggesting that the BDNF-induced transient increase of Ca(2+) through the activation of the PLC-gamma/ IP(3) pathway was essential for the glutamate release. We found that BDNF induced a Na(+) influx. This was blocked by treatment with TTX. U-73122 and xestospongin C blocked the BDNF-induced Na(+) influx, suggesting that the Na(+)influx required the BDNF-induced Ca(2+) increase. Next, we examined the possibility that a co-transporter of Na(+) and glutamate was involved in the BDNF-induced glutamate release. BDNF-induced glutamate release was blocked by L-trans-pyrollidine-2,4-dicalboxylic acid (t-PDC), a glutamate transporter inhibitor, whereas neither the 4-aminopyridine (4AP)- nor high potassium (HK(+))-induced release was blocked by t-PDC. In addition, DL-threo-beta-benzyloxyaspartate (DL-TBOA) also blocked the BDNF-mediated glutamate release, suggesting that reverse transport of glutamate may be involved. All the results therefore suggest that Na(+)-dependent reverse transport contributes to BDNF-mediated transmitter release through the PLC-gamma/IP(3)-mediated Ca(2+) signaling. | lld:pubmed |
| pubmed-article:11599006 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11599006 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11599006 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11599006 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11599006 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11599006 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:11599006 | pubmed:issn | 0360-4012 | lld:pubmed |
| pubmed-article:11599006 | pubmed:author | pubmed-author:MatsumotoTT | lld:pubmed |
| pubmed-article:11599006 | pubmed:author | pubmed-author:HatanakaHH | lld:pubmed |
| pubmed-article:11599006 | pubmed:author | pubmed-author:KojimaMM | lld:pubmed |
| pubmed-article:11599006 | pubmed:author | pubmed-author:AdachiNN | lld:pubmed |
| pubmed-article:11599006 | pubmed:author | pubmed-author:TakeiNN | lld:pubmed |
| pubmed-article:11599006 | pubmed:author | pubmed-author:NumakawaTT | lld:pubmed |
| pubmed-article:11599006 | pubmed:author | pubmed-author:YokomakuDD | lld:pubmed |
| pubmed-article:11599006 | pubmed:copyrightInfo | Copyright 2001 Wiley-Liss, Inc. | lld:pubmed |
| pubmed-article:11599006 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11599006 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:11599006 | pubmed:volume | 66 | lld:pubmed |
| pubmed-article:11599006 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11599006 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11599006 | pubmed:pagination | 96-108 | lld:pubmed |
| pubmed-article:11599006 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:11599006 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11599006 | pubmed:articleTitle | Brain-derived neurotrophic factor triggers a rapid glutamate release through increase of intracellular Ca(2+) and Na(+) in cultured cerebellar neurons. | lld:pubmed |
| pubmed-article:11599006 | pubmed:affiliation | Division of Protein Biosynthesis, Institute for Protein Research, Osaka University, Suita, Osaka, Japan. numakawa@protein.osaka-u.ac.jp | lld:pubmed |
| pubmed-article:11599006 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11599006 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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