rdf:type |
|
lifeskim:mentions |
umls-concept:C0004461,
umls-concept:C0007765,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0086045,
umls-concept:C0178719,
umls-concept:C0333799,
umls-concept:C0439799,
umls-concept:C0441472,
umls-concept:C0596235,
umls-concept:C1709059
|
pubmed:dateCreated |
2000-1-4
|
pubmed:abstractText |
1. Action potential-evoked [Ca2+]i rises in basket cell axons of rat cerebellar slices were studied using two-photon laser scanning microscopy and whole-cell recording, to identify the K+ channels controlling the shape of the axonal action potential. 2. Whole-cell recordings of Purkinje cell IPSCs were used to screen K+ channel subtypes which could contribute to axonal repolarization. alpha-Dendrotoxin, 4-aminopyridine, charybdotoxin and tetraethylammonium chloride increased IPSC rate and/or amplitude, whereas iberiotoxin and apamin failed to affect the IPSCs. 3. The effects of those K+ channel blockers that enhanced transmitter release on the [Ca2+]i rises elicited in basket cell axons by action potentials fell into three groups: 4-aminopyridine strongly increased action potential-evoked [Ca2+]i; tetraethylammonium and charybdotoxin were ineffective alone but augmented the effects of 4-aminopyridine; alpha-dendrotoxin had no effect. 4. We conclude that cerebellar basket cells contain at least three pharmacologically distinct K+ channels, which regulate transmitter release through different mechanisms. 4-Aminopyridine-sensitive, alpha-dendrotoxin-insensitive K+ channels are mainly responsible for repolarization in basket cell presynaptic terminals. K+ channels blocked by charybdotoxin and tetraethylammonium have a minor role in repolarization. alpha-Dendrotoxin-sensitive channels are not involved in shaping the axonal action potential waveform. The two last types of channels must therefore exert control of synaptic activity through a pathway unrelated to axonal action potential broadening.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-10024354,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-10191303,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-10517792,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-1497894,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-1673717,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-1988937,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-2555158,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-7508581,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-7612860,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-7837096,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-8046438,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-8120636,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-8158277,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-8361541,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-8558264,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-8563969,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-8601803,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-8606791,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-8794077,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-8814615,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-8821131,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-8915580,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-9202119,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-9206549,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-9457476,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/10517801-9863670
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pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
0022-3751
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
1
|
pubmed:volume |
520 Pt 1
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
65-78
|
pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:10517801-4-Aminopyridine,
pubmed-meshheading:10517801-Action Potentials,
pubmed-meshheading:10517801-Animals,
pubmed-meshheading:10517801-Axons,
pubmed-meshheading:10517801-Calcium,
pubmed-meshheading:10517801-Cerebellum,
pubmed-meshheading:10517801-Elapid Venoms,
pubmed-meshheading:10517801-Electrophysiology,
pubmed-meshheading:10517801-Excitatory Postsynaptic Potentials,
pubmed-meshheading:10517801-Neurotoxins,
pubmed-meshheading:10517801-Patch-Clamp Techniques,
pubmed-meshheading:10517801-Potassium Channel Blockers,
pubmed-meshheading:10517801-Potassium Channels,
pubmed-meshheading:10517801-Presynaptic Terminals,
pubmed-meshheading:10517801-Purkinje Cells,
pubmed-meshheading:10517801-Rats
|
pubmed:year |
1999
|
pubmed:articleTitle |
Modulation by K+ channels of action potential-evoked intracellular Ca2+ concentration rises in rat cerebellar basket cell axons.
|
pubmed:affiliation |
Arbeitsgruppe Zellulare Neurobiologie, Max-Planck-Institut fur biophysikalische Chemie, Am Fassberg, D-37070 Gottingen, Germany.
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pubmed:publicationType |
Journal Article,
In Vitro
|