Source:http://linkedlifedata.com/resource/pubmed/id/10414968
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
15
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pubmed:dateCreated |
1999-8-16
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pubmed:abstractText |
The symptoms of Parkinson disease are thought to result in part from increased burst activity in globus pallidus neurons. To gain a better understanding of the factors governing this activity, we studied delayed rectifier K(+) conductances in acutely isolated rat globus pallidus (GP) neurons, using whole-cell voltage-clamp and single-cell RT-PCR techniques. From a holding potential of -40 mV, depolarizing voltage steps in identified GP neurons evoked slowly inactivating K(+) currents. Analysis of the tail currents revealed rapidly and slowly deactivating currents of similar amplitude. The fast component of the current deactivated with a time constant of 11. 1 +/- 0.8 msec at -40 mV and was blocked by micromolar concentrations of 4-AP and TEA (K(D) approximately 140 microM). The slow component of the current deactivated with a time constant of 89 +/- 10 microseconds at -40 mV and was less sensitive to TEA (K(D) = 0.8 mM) and 4-AP (K(D) approximately 6 mM). Organic antagonists of Kv1 family channels had little or no effect on somatic currents. These properties are consistent with the hypothesis that the rapidly deactivating current is attributable to Kv3.1/3.2 channels and the slowly deactivating current to Kv2.1-containing channels. Semiquantitative single-cell RT-PCR analysis of Kv3 and Kv2 family mRNAs supported this conclusion. An alteration in the balance of these two channel types could underlie the emergence of burst firing after dopamine-depleting lesions.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/4-Aminopyridine,
http://linkedlifedata.com/resource/pubmed/chemical/Delayed Rectifier Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Kcnb1 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Neuropeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, Voltage-Gated,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Shab Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Shaw Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Tetraethylammonium
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0270-6474
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
19
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6394-404
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10414968-4-Aminopyridine,
pubmed-meshheading:10414968-Animals,
pubmed-meshheading:10414968-Delayed Rectifier Potassium Channels,
pubmed-meshheading:10414968-Electric Conductivity,
pubmed-meshheading:10414968-Globus Pallidus,
pubmed-meshheading:10414968-Neurons,
pubmed-meshheading:10414968-Neuropeptides,
pubmed-meshheading:10414968-Potassium Channel Blockers,
pubmed-meshheading:10414968-Potassium Channels,
pubmed-meshheading:10414968-Potassium Channels, Voltage-Gated,
pubmed-meshheading:10414968-RNA, Messenger,
pubmed-meshheading:10414968-Rats,
pubmed-meshheading:10414968-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:10414968-Shab Potassium Channels,
pubmed-meshheading:10414968-Shaw Potassium Channels,
pubmed-meshheading:10414968-Tetraethylammonium
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pubmed:year |
1999
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pubmed:articleTitle |
Delayed rectifier currents in rat globus pallidus neurons are attributable to Kv2.1 and Kv3.1/3.2 K(+) channels.
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pubmed:affiliation |
Department of Physiology/Northwestern University Institute for Neuroscience, Northwestern University Medical School, Chicago, Illinois 60611, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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