Large conductance Ca(2+)-activated K+ channels are involved in both spike shaping and firing regulation in Helix neurones.
Identifieur interne : 000212 ( Pmc/Curation ); précédent : 000211; suivant : 000213Large conductance Ca(2+)-activated K+ channels are involved in both spike shaping and firing regulation in Helix neurones.
Auteurs : M. Crest ; M. GolaSource :
- The Journal of Physiology [ 0022-3751 ] ; 1993.
Abstract
1. The role of BK-type calcium-dependent K+ channels (K+Ca) in cell firing regulation was evaluated by performing whole-cell voltage clamp and patch clamp experiments on the U cell neurones in the snail Helix pomatia. These cells were selected because most of the repolarizing K+ current flowed through K+Ca channels. 2. U cells generated overshooting Ca(2+)-dependent spikes in Na(+)-free saline. In response to prolonged depolarizing current, they fired a limited number of spikes of decreasing amplitude, and behaved like fast-adapting or phasic neurones. 3. Under voltage clamp conditions, the K+Ca current had a slow onset at voltages that induced small Ca2+ entries. By manipulating the Ca2+ entry (either with appropriate voltage programmes or by changing the Ca2+ content of the bath), the K+Ca channel opening was found to be rate limited by the Ca2+ binding step and not by the voltage-dependent conformational change to the open state. 4. Despite the slow activation rate observed in voltage-clamped cells, 25-30% of the available K+Ca current was found to be active during isolated spikes. These data were based on patch clamp, spike-like voltage clamp and hybrid current clamp-voltage clamp experiments. 5. The fact that spikes led the slowly rising K+Ca current to shift into a fast activating mode was accounted for by the large surge of Ca2+ current concomitant with spike upstroke. The early calcium surge resulted in local increases in cytosolic calcium, which speeded up the binding of calcium ions to the closed K+Ca channels. From changes in the null Ca2+ current voltage, it was calculated that the submembrane [Ca2+]i increase to 50-80 microM during the spike. 6. Due to their fast voltage dependence, K+Ca channels appeared to play no role in shaping the interspike trajectory. 7. Even in the fast activating mode, the K+Ca current had a finite rate of rise and was not involved in repolarizing short duration Na(+-dependent action potentials. The current became more and more active, however, when voltage-gated K+ channels were progressively inactivated during firing. 8. The fast adaptation exhibited by U cells upon sustained depolarization was not paralleled by a recruitment of K+Ca channels because of the cumulative Ca2+ entries. During a spike burst, the K+Ca current progressively overlapped the depolarizing Ca2+ current, which ultimately stopped the firing. The early opening of K+Ca channels was ascribed to residual Ca2+ accumulation that kept part of the channels in the Ca(2+)-bound state ready to be opened quickly by cell depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)
Url:
PubMed: 8229836
PubMed Central: 1175429
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<author><name sortKey="Crest, M" sort="Crest, M" uniqKey="Crest M" first="M" last="Crest">M. Crest</name>
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<author><name sortKey="Gola, M" sort="Gola, M" uniqKey="Gola M" first="M" last="Gola">M. Gola</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Large conductance Ca(2+)-activated K+ channels are involved in both spike shaping and firing regulation in Helix neurones.</title>
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<author><name sortKey="Gola, M" sort="Gola, M" uniqKey="Gola M" first="M" last="Gola">M. Gola</name>
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<series><title level="j">The Journal of Physiology</title>
<idno type="ISSN">0022-3751</idno>
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<front><div type="abstract" xml:lang="en"><p>1. The role of BK-type calcium-dependent K+ channels (K+Ca) in cell firing regulation was evaluated by performing whole-cell voltage clamp and patch clamp experiments on the U cell neurones in the snail Helix pomatia. These cells were selected because most of the repolarizing K+ current flowed through K+Ca channels. 2. U cells generated overshooting Ca(2+)-dependent spikes in Na(+)-free saline. In response to prolonged depolarizing current, they fired a limited number of spikes of decreasing amplitude, and behaved like fast-adapting or phasic neurones. 3. Under voltage clamp conditions, the K+Ca current had a slow onset at voltages that induced small Ca2+ entries. By manipulating the Ca2+ entry (either with appropriate voltage programmes or by changing the Ca2+ content of the bath), the K+Ca channel opening was found to be rate limited by the Ca2+ binding step and not by the voltage-dependent conformational change to the open state. 4. Despite the slow activation rate observed in voltage-clamped cells, 25-30% of the available K+Ca current was found to be active during isolated spikes. These data were based on patch clamp, spike-like voltage clamp and hybrid current clamp-voltage clamp experiments. 5. The fact that spikes led the slowly rising K+Ca current to shift into a fast activating mode was accounted for by the large surge of Ca2+ current concomitant with spike upstroke. The early calcium surge resulted in local increases in cytosolic calcium, which speeded up the binding of calcium ions to the closed K+Ca channels. From changes in the null Ca2+ current voltage, it was calculated that the submembrane [Ca2+]i increase to 50-80 microM during the spike. 6. Due to their fast voltage dependence, K+Ca channels appeared to play no role in shaping the interspike trajectory. 7. Even in the fast activating mode, the K+Ca current had a finite rate of rise and was not involved in repolarizing short duration Na(+-dependent action potentials. The current became more and more active, however, when voltage-gated K+ channels were progressively inactivated during firing. 8. The fast adaptation exhibited by U cells upon sustained depolarization was not paralleled by a recruitment of K+Ca channels because of the cumulative Ca2+ entries. During a spike burst, the K+Ca current progressively overlapped the depolarizing Ca2+ current, which ultimately stopped the firing. The early opening of K+Ca channels was ascribed to residual Ca2+ accumulation that kept part of the channels in the Ca(2+)-bound state ready to be opened quickly by cell depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)</p>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Physiol</journal-id>
<journal-title>The Journal of Physiology</journal-title>
<issn pub-type="ppub">0022-3751</issn>
<issn pub-type="epub">1469-7793</issn>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">8229836</article-id>
<article-id pub-id-type="pmc">1175429</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Large conductance Ca(2+)-activated K+ channels are involved in both spike shaping and firing regulation in Helix neurones.</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Crest</surname>
<given-names>M</given-names>
</name>
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<contrib contrib-type="author"><name><surname>Gola</surname>
<given-names>M</given-names>
</name>
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<aff>Laboratoire de Neurobiologie, CNRS, Marseille, France.</aff>
<pub-date pub-type="ppub"><month>6</month>
<year>1993</year>
</pub-date>
<volume>465</volume>
<fpage>265</fpage>
<lpage>287</lpage>
<abstract><p>1. The role of BK-type calcium-dependent K+ channels (K+Ca) in cell firing regulation was evaluated by performing whole-cell voltage clamp and patch clamp experiments on the U cell neurones in the snail Helix pomatia. These cells were selected because most of the repolarizing K+ current flowed through K+Ca channels. 2. U cells generated overshooting Ca(2+)-dependent spikes in Na(+)-free saline. In response to prolonged depolarizing current, they fired a limited number of spikes of decreasing amplitude, and behaved like fast-adapting or phasic neurones. 3. Under voltage clamp conditions, the K+Ca current had a slow onset at voltages that induced small Ca2+ entries. By manipulating the Ca2+ entry (either with appropriate voltage programmes or by changing the Ca2+ content of the bath), the K+Ca channel opening was found to be rate limited by the Ca2+ binding step and not by the voltage-dependent conformational change to the open state. 4. Despite the slow activation rate observed in voltage-clamped cells, 25-30% of the available K+Ca current was found to be active during isolated spikes. These data were based on patch clamp, spike-like voltage clamp and hybrid current clamp-voltage clamp experiments. 5. The fact that spikes led the slowly rising K+Ca current to shift into a fast activating mode was accounted for by the large surge of Ca2+ current concomitant with spike upstroke. The early calcium surge resulted in local increases in cytosolic calcium, which speeded up the binding of calcium ions to the closed K+Ca channels. From changes in the null Ca2+ current voltage, it was calculated that the submembrane [Ca2+]i increase to 50-80 microM during the spike. 6. Due to their fast voltage dependence, K+Ca channels appeared to play no role in shaping the interspike trajectory. 7. Even in the fast activating mode, the K+Ca current had a finite rate of rise and was not involved in repolarizing short duration Na(+-dependent action potentials. The current became more and more active, however, when voltage-gated K+ channels were progressively inactivated during firing. 8. The fast adaptation exhibited by U cells upon sustained depolarization was not paralleled by a recruitment of K+Ca channels because of the cumulative Ca2+ entries. During a spike burst, the K+Ca current progressively overlapped the depolarizing Ca2+ current, which ultimately stopped the firing. The early opening of K+Ca channels was ascribed to residual Ca2+ accumulation that kept part of the channels in the Ca(2+)-bound state ready to be opened quickly by cell depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)</p>
</abstract>
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