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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
Pt 2
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pubmed:dateCreated |
2003-1-15
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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.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-10627581,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-10675775,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-10675916,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-10915629,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-11032899,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-11313432,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-11707360,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-1323145,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-1352806,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-1654231,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-1665109,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-1822537,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-2885073,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-4044917,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-7521083,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-7832825,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-7901765,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-7902110,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-7993635,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-8014856,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-8382501,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-8787136,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-8849448,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-9065864,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-9122253,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-9334432,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-9535573,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-9539805,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-9575291,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-9581770,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-9651201,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-9698323,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12527734-9880593
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
546
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
483-90
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:12527734-Agatoxins,
pubmed-meshheading:12527734-Aging,
pubmed-meshheading:12527734-Animals,
pubmed-meshheading:12527734-Animals, Newborn,
pubmed-meshheading:12527734-Calcium Channel Blockers,
pubmed-meshheading:12527734-Cholinergic Fibers,
pubmed-meshheading:12527734-Corpus Striatum,
pubmed-meshheading:12527734-Dopamine,
pubmed-meshheading:12527734-Dopamine Agonists,
pubmed-meshheading:12527734-Interneurons,
pubmed-meshheading:12527734-Neural Inhibition,
pubmed-meshheading:12527734-Quinpirole,
pubmed-meshheading:12527734-Rats,
pubmed-meshheading:12527734-Spider Venoms,
pubmed-meshheading:12527734-Synaptic Transmission,
pubmed-meshheading:12527734-gamma-Aminobutyric Acid,
pubmed-meshheading:12527734-omega-Conotoxin GVIA
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pubmed:year |
2003
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pubmed:articleTitle |
Parallel decrease in omega-conotoxin-sensitive transmission and dopamine-induced inhibition at the striatal synapse of developing rats.
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pubmed:affiliation |
Division of Cerebral Structure, National Institute for Physiological Sciences, Myodaiji, Okazaki 444-8585, Japan. tmomi@nips.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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