| pubmed-article:12527734 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12527734 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:12527734 | lifeskim:mentions | umls-concept:C0039062 | lld:lifeskim |
| pubmed-article:12527734 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:12527734 | lifeskim:mentions | umls-concept:C1521797 | lld:lifeskim |
| pubmed-article:12527734 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:12527734 | lifeskim:mentions | umls-concept:C0547047 | lld:lifeskim |
| pubmed-article:12527734 | lifeskim:mentions | umls-concept:C2348042 | lld:lifeskim |
| pubmed-article:12527734 | pubmed:issue | Pt 2 | lld:pubmed |
| pubmed-article:12527734 | pubmed:dateCreated | 2003-1-15 | lld:pubmed |
| pubmed-article:12527734 | pubmed:abstractText | Whole-cell patch-clamp recordings of GABAergic IPSCs were made from cholinergic interneurones in slices of striatum from developing rats aged 21-60 days postnatal. In addition, the Ca(2+) channel subtypes involved in synaptic transmission, as well as dopamine (DA)-induced presynaptic inhibition, were investigated pharmacologically with development by bath application of Ca(2+) channel blockers and DA receptor agonists. The IPSC amplitude was reduced by omega-conotoxin GVIA (omega-CgTX) or omega-agatoxin TK (omega-Aga-TK) across the whole age range, suggesting that multiple types of Ca(2+) channels mediate transmission of the synapse. The IPSC fraction reduced by omega-CgTX significantly decreased, whereas that reduced by omega-Aga-TK remained unchanged with development. DA or quinpirole, a D(2)-like receptor agonist, presynaptically reduced the IPSC amplitude throughout development. The DA-induced inhibition decreased with age in parallel with the decrease in N-type Ca(2+) channels. DA showed no further inhibition of IPSCs after the inhibitory effect of omega-CgTX had reached steady state throughout development. These results demonstrate that there is a functional link between presynaptic N-type Ca(2+) channels and D(2)-like DA receptors at inhibitory synapses in the striatum. They also demonstrate that the suppression of GABAergic transmission by D(2)-like receptors is mediated by modulation of N-type Ca(2+) channels and decreases in parallel with the developmental decline in the contribution of N-type Ca(2+) channels to exocytosis. | lld:pubmed |
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| pubmed-article:12527734 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12527734 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12527734 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12527734 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12527734 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:12527734 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:12527734 | pubmed:author | pubmed-author:MomiyamaToshi... | lld:pubmed |
| pubmed-article:12527734 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12527734 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:12527734 | pubmed:volume | 546 | lld:pubmed |
| pubmed-article:12527734 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12527734 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12527734 | pubmed:pagination | 483-90 | lld:pubmed |
| pubmed-article:12527734 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:12527734 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12527734 | pubmed:articleTitle | Parallel decrease in omega-conotoxin-sensitive transmission and dopamine-induced inhibition at the striatal synapse of developing rats. | lld:pubmed |
| pubmed-article:12527734 | pubmed:affiliation | Division of Cerebral Structure, National Institute for Physiological Sciences, Myodaiji, Okazaki 444-8585, Japan. tmomi@nips.ac.jp | lld:pubmed |
| pubmed-article:12527734 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12527734 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:12527734 | lld:pubmed |
