| pubmed-article:994042 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:994042 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:994042 | lifeskim:mentions | umls-concept:C0032821 | lld:lifeskim |
| pubmed-article:994042 | lifeskim:mentions | umls-concept:C0037378 | lld:lifeskim |
| pubmed-article:994042 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:994042 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
| pubmed-article:994042 | lifeskim:mentions | umls-concept:C0205421 | lld:lifeskim |
| pubmed-article:994042 | lifeskim:mentions | umls-concept:C0998124 | lld:lifeskim |
| pubmed-article:994042 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:994042 | pubmed:dateCreated | 1977-1-29 | lld:pubmed |
| pubmed-article:994042 | pubmed:abstractText | The net outward current in bursting pace-maker neurones of the snail (Helix pomatia) during sustained and repeated voltage clamp pulses was studied. The properties of currents remaining in cobalt-Ringer or after TEA injection were compared with those in untreated cells. 2. With sustained voltage clamp depolarizations the net outward current first increases to a maximum at 150 msec and then declines to 60% or less of its peak intensity. This depression, which is greater during repetition of short pulses (e.g. 100 msec pulses at 0-5 sec intervals), represents a true decrease in the outward flow of K (designated IK) and is not due to a decreased driving force resulting from extracellular K accumulation. The steady-state current-voltage (I-V) relationship for IK is N-shaped (Heyer & Lux, 1976). 3. A component of IK persists when Ca and Mg in the medium are replaced by Co (ICo-res). With voltage clamp depolarizations ICo-res increases rapidly to a maximum and then partially inactivates with voltage dependent time constants of hundredths or tenths of seconds. Repolarization removes the inactivation. Thus, repeated stimulation with short pulses does not increase the depression of ICo-res-ICo-res (e.g. measured during voltage steps from holding potentials of -50 to near 0 mV) is smaller in test pulses preceded by depolarization and larger in pulses preceded by hyperpolarization. The steady state I-V relationship is not N-shaped. ICo-res is blocked by intracellular injection of tetraethylammonium (TEA). 4. Repeated voltage clamp depolarization to near 0 mV with 100 msec pulses for neurones with large Ca currents in normal Ringer produces a long-term depression which is maximal with 300-400 msec repolarizations (to -50 mV) between pulses. This corresponds with stimulus parameters for the maximum Ca current (Heyer & Lux, 1976). Intracellular injection of Ca2+ (also Ba2+ and Co2+) likewise reduces the total net outward current and especially the delayed outward current under voltage clamp. 5. The component of IK which is removed by Co is identified as Ca dependent and designated IK(Ca). With single voltage clamp pulses IK(Ca) follows the approximate time course and voltage dependence of the slow inward Ca current (Iin slow; Heyer & Lux, 1976). Several lines of evidence suggest that Ca ions moving through the membrane activate IK(Ca). 6. Part of IK cannot be blocked by intracellular TEA injection. In different neurones the magnitude of the IK component resistant to TEA (ITEA-res) is approximately proportional to the relative magnitudes of Iin slow.ITEA-res does not inactivate with sustained depolarization and shows pronounced long-term depression with repetitive stimulation at intermediate intervals and an increased outward current at the onset of the second and subsequent pulses following short repolarizations. The steady-state I-V relationship is N-shaped. ITEA-res is abolished by extracellular Co. 7. A net inward current with low depolarizations can be measured after TEA injection... | lld:pubmed |
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| pubmed-article:994042 | pubmed:language | eng | lld:pubmed |
| pubmed-article:994042 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:994042 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:994042 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:994042 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:994042 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:994042 | pubmed:author | pubmed-author:LuxH DHD | lld:pubmed |
| pubmed-article:994042 | pubmed:author | pubmed-author:HeyenC FCF | lld:pubmed |
| pubmed-article:994042 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:994042 | pubmed:volume | 262 | lld:pubmed |
| pubmed-article:994042 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:994042 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:994042 | pubmed:pagination | 349-82 | lld:pubmed |
| pubmed-article:994042 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:994042 | pubmed:year | 1976 | lld:pubmed |
| pubmed-article:994042 | pubmed:articleTitle | Control of the delayed outward potassium currents in bursting pace-maker neurones of the snail, Helix pomatia. | lld:pubmed |
| pubmed-article:994042 | pubmed:publicationType | Journal Article | lld:pubmed |
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