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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells</title>
<author><name sortKey="Lenz, R A" sort="Lenz, R A" uniqKey="Lenz R" first="R A" last="Lenz">R A Lenz</name>
</author>
<author><name sortKey="Wagner, J J" sort="Wagner, J J" uniqKey="Wagner J" first="J J" last="Wagner">J J Wagner</name>
</author>
<author><name sortKey="Alger, B E" sort="Alger, B E" uniqKey="Alger B" first="B E" last="Alger">B E Alger</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">9729617</idno>
<idno type="pmc">2231194</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2231194</idno>
<idno type="RBID">PMC:2231194</idno>
<idno type="doi">10.1111/j.1469-7793.1998.061bf.x</idno>
<date when="1998">1998</date>
<idno type="wicri:Area/Pmc/Corpus">000318</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000318</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells</title>
<author><name sortKey="Lenz, R A" sort="Lenz, R A" uniqKey="Lenz R" first="R A" last="Lenz">R A Lenz</name>
</author>
<author><name sortKey="Wagner, J J" sort="Wagner, J J" uniqKey="Wagner J" first="J J" last="Wagner">J J Wagner</name>
</author>
<author><name sortKey="Alger, B E" sort="Alger, B E" uniqKey="Alger B" first="B E" last="Alger">B E Alger</name>
</author>
</analytic>
<series><title level="j">The Journal of Physiology</title>
<idno type="ISSN">0022-3751</idno>
<idno type="eISSN">1469-7793</idno>
<imprint><date when="1998">1998</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p><list list-type="order"><list-item><p>We investigated depolarization-induced suppression of inhibition (DSI) under whole-cell voltage clamp in CA1 pyramidal neurons of rat hippocampal slices. DSI, a transient reduction in monosynaptic evoked GABA<sub>A</sub>
ergic IPSCs lasting for ∼1 min, was induced by depolarizing the pyramidal cell to −10 or 0 mV for 1 or 2 s.</p>
</list-item>
<list-item><p>Raising extracellular Ca<sup>2+</sup>
concentration increased DSI, and varying the DSI-inducing voltage step showed that the voltage dependence of DSI was like that of high-voltage-activated Ca<sup>2+</sup>
channels.</p>
</list-item>
<list-item><p>The P- and Q-type Ca<sup>2+</sup>
channel blocker ω-agatoxin TK (200 n<sc>m</sc>
and 1 μ<sc>m</sc>
) and the R- and T-type Ca<sup>2+</sup>
channel blocker Ni<sup>2+</sup>
(100 μ<sc>m</sc>
) reduced IPSCs without reducing DSI.</p>
</list-item>
<list-item><p>The specific N-type Ca<sup>2+</sup>
channel antagonist ω-conotoxin GVIA (250 n<sc>m</sc>
) reduced IPSC amplitudes and almost completely abolished DSI.</p>
</list-item>
<list-item><p>Blocking L-type Ca<sup>2+</sup>
channels with nifedipine (10 μ<sc>m</sc>
) had no effect on IPSCs or DSI induced by our standard protocol, but reduced DSI induced by the unclamped Na<sup>+</sup>
- and Ca<sup>2+</sup>
-dependent spikes that occurred when 2(triethylamino)-<italic>N-</italic>
(2,6-dimethylphenyl)acetamide (QX-314) was omitted from the recording pipette solution.</p>
</list-item>
<list-item><p>Although intracellular Ca<sup>2+</sup>
stores were not measured, DSI was not affected by cyclopiazonic acid (CPA, 20–40 μ<sc>m</sc>
), a blocker of Ca<sup>2+</sup>
uptake into intracellular stores.</p>
</list-item>
<list-item><p>We conclude that DSI is initiated by Ca<sup>2+</sup>
influx through N- and, under certain conditions, L-type Ca<sup>2+</sup>
channels.</p>
</list-item>
</list>
</p>
</div>
</front>
</TEI>
<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-id journal-id-type="publisher-id">tjp</journal-id>
<journal-title>The Journal of Physiology</journal-title>
<issn pub-type="ppub">0022-3751</issn>
<issn pub-type="epub">1469-7793</issn>
<publisher><publisher-name>Blackwell Science Inc</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">9729617</article-id>
<article-id pub-id-type="pmc">2231194</article-id>
<article-id pub-id-type="doi">10.1111/j.1469-7793.1998.061bf.x</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Original Articles</subject>
</subj-group>
</article-categories>
<title-group><article-title>N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Lenz</surname>
<given-names>R A</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Wagner</surname>
<given-names>J J</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Alger</surname>
<given-names>B E</given-names>
</name>
</contrib>
<aff><institution>Department of Physiology, University of Maryland School of Medicine</institution>
<addr-line>Baltimore, MD 21201, USA</addr-line>
</aff>
</contrib-group>
<author-notes><corresp id="cor1"><bold>Corresponding author</bold>
B. E. Alger: Department of Physiology, University of Maryland School of Medicine, 655 West Baltimore Street, Baltimore, MD 21201, USA. Email: <email>balger@umaryland.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><day>01</day>
<month>10</month>
<year>1998</year>
</pub-date>
<volume>512</volume>
<issue>Pt 1</issue>
<fpage>61</fpage>
<lpage>73</lpage>
<history><date date-type="received"><day>02</day>
<month>3</month>
<year>1998</year>
</date>
<date date-type="accepted"><day>25</day>
<month>6</month>
<year>1998</year>
</date>
</history>
<copyright-statement>© The Physiological Society 1998</copyright-statement>
<copyright-year>1998</copyright-year>
<abstract><p><list list-type="order"><list-item><p>We investigated depolarization-induced suppression of inhibition (DSI) under whole-cell voltage clamp in CA1 pyramidal neurons of rat hippocampal slices. DSI, a transient reduction in monosynaptic evoked GABA<sub>A</sub>
ergic IPSCs lasting for ∼1 min, was induced by depolarizing the pyramidal cell to −10 or 0 mV for 1 or 2 s.</p>
</list-item>
<list-item><p>Raising extracellular Ca<sup>2+</sup>
concentration increased DSI, and varying the DSI-inducing voltage step showed that the voltage dependence of DSI was like that of high-voltage-activated Ca<sup>2+</sup>
channels.</p>
</list-item>
<list-item><p>The P- and Q-type Ca<sup>2+</sup>
channel blocker ω-agatoxin TK (200 n<sc>m</sc>
and 1 μ<sc>m</sc>
) and the R- and T-type Ca<sup>2+</sup>
channel blocker Ni<sup>2+</sup>
(100 μ<sc>m</sc>
) reduced IPSCs without reducing DSI.</p>
</list-item>
<list-item><p>The specific N-type Ca<sup>2+</sup>
channel antagonist ω-conotoxin GVIA (250 n<sc>m</sc>
) reduced IPSC amplitudes and almost completely abolished DSI.</p>
</list-item>
<list-item><p>Blocking L-type Ca<sup>2+</sup>
channels with nifedipine (10 μ<sc>m</sc>
) had no effect on IPSCs or DSI induced by our standard protocol, but reduced DSI induced by the unclamped Na<sup>+</sup>
- and Ca<sup>2+</sup>
-dependent spikes that occurred when 2(triethylamino)-<italic>N-</italic>
(2,6-dimethylphenyl)acetamide (QX-314) was omitted from the recording pipette solution.</p>
</list-item>
<list-item><p>Although intracellular Ca<sup>2+</sup>
stores were not measured, DSI was not affected by cyclopiazonic acid (CPA, 20–40 μ<sc>m</sc>
), a blocker of Ca<sup>2+</sup>
uptake into intracellular stores.</p>
</list-item>
<list-item><p>We conclude that DSI is initiated by Ca<sup>2+</sup>
influx through N- and, under certain conditions, L-type Ca<sup>2+</sup>
channels.</p>
</list-item>
</list>
</p>
</abstract>
</article-meta>
</front>
</pmc>
</record>
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