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rdf:type |
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lifeskim:mentions |
umls-concept:C0006685,
umls-concept:C0007765,
umls-concept:C0030685,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0039062,
umls-concept:C0391871,
umls-concept:C0680255,
umls-concept:C1273518,
umls-concept:C1283071,
umls-concept:C1707723,
umls-concept:C1963578
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pubmed:issue |
2
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pubmed:dateCreated |
1994-9-1
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pubmed:abstractText |
The effects of calcium channel blockers on potassium-induced transmitter release were studied in thin slices of cerebellum from neonatal rats using whole-cell patch clamp methods. Miniature inhibitory postsynaptic currents (mIPSCs) mediated by gamma-aminobutyric acid (GABA) were recorded from deep cerebellar nuclear neurones in the presence of tetrodotoxin. The frequency of mIPSCs was reproducibly increased by a brief application of high-potassium solution. In the presence of the L-type Ca2+ channel blocker nicardipine (10 microM), the potassium-induced increase in mIPSC frequency was suppressed by 49%. Neither the mean amplitude nor the time course of mIPSCs was affected by the blocker. The N-type Ca2+ channel blocker omega-conotoxin GVIA (omega-CgTX, 3 microM) had no effect on the frequency of potassium-induced mIPSCs. The P-type Ca2+ channel blocker omega-Aga-IVA (200 nM) suppressed the potassium-induced increase in mIPSC frequency by 83% without affecting the mean amplitude or time course of mIPSCs. Comparing these data with previous studies of neurally evoked transmission, it is concluded that the Ca2+ channel subtypes responsible for potassium-induced transmitter release may be different from those mediating fast synaptic transmission.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-1321648,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-1357749,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-1432720,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-1684901,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-1707966,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-1980068,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-2428039,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-2432656,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-2451016,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-2537980,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-2547195,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-2780225,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-4078752,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-6065887,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7913967-7901765
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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 |
Apr
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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 |
476
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
197-202
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:7913967-Animals,
pubmed-meshheading:7913967-Animals, Newborn,
pubmed-meshheading:7913967-Calcium Channel Blockers,
pubmed-meshheading:7913967-Calcium Channels,
pubmed-meshheading:7913967-Cerebellum,
pubmed-meshheading:7913967-Dihydropyridines,
pubmed-meshheading:7913967-Membrane Potentials,
pubmed-meshheading:7913967-Neurons,
pubmed-meshheading:7913967-Neurotransmitter Agents,
pubmed-meshheading:7913967-Peptides,
pubmed-meshheading:7913967-Potassium,
pubmed-meshheading:7913967-Rats,
pubmed-meshheading:7913967-Rats, Wistar,
pubmed-meshheading:7913967-Spider Venoms,
pubmed-meshheading:7913967-Synapses,
pubmed-meshheading:7913967-omega-Agatoxin IVA,
pubmed-meshheading:7913967-omega-Conotoxin GVIA
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pubmed:year |
1994
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pubmed:articleTitle |
Calcium channels responsible for potassium-induced transmitter release at rat cerebellar synapses.
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pubmed:affiliation |
Department of Physiology, Kyoto University Faculty of Medicine, Japan.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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