N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells.
Identifieur interne : 000C76 ( Main/Exploration ); précédent : 000C75; suivant : 000C77N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells.
Auteurs : R A Lenz [États-Unis] ; J J Wagner ; B E AlgerSource :
- The Journal of physiology [ 0022-3751 ] ; 1998.
English descriptors
- KwdEn :
- Animals, Calcium (metabolism), Calcium Channel Blockers (pharmacology), Calcium Channels (drug effects), Calcium Channels (physiology), Calcium Channels, L-Type, Evoked Potentials (drug effects), Evoked Potentials (physiology), Hippocampus (physiology), In Vitro Techniques, Indoles (pharmacology), Lidocaine (analogs & derivatives), Lidocaine (pharmacology), Male, Nickel (pharmacology), Nifedipine (pharmacology), Peptides (pharmacology), Pyramidal Cells (drug effects), Pyramidal Cells (physiology), Rats, Rats, Sprague-Dawley, omega-Conotoxin GVIA.
- MESH :
- chemical , analogs & derivatives : Lidocaine.
- chemical , drug effects : Calcium Channels.
- chemical , metabolism : Calcium.
- chemical , pharmacology : Calcium Channel Blockers, Indoles, Lidocaine, Nickel, Nifedipine, Peptides.
- chemical , physiology : Calcium Channels.
- drug effects : Evoked Potentials, Pyramidal Cells.
- physiology : Evoked Potentials, Hippocampus, Pyramidal Cells.
- Animals, Calcium Channels, L-Type, In Vitro Techniques, Male, Rats, Rats, Sprague-Dawley, omega-Conotoxin GVIA.
Abstract
1. 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 GABAAergic IPSCs lasting for approximately 1 min, was induced by depolarizing the pyramidal cell to -10 or 0 mV for 1 or 2 s. 2. Raising extracellular Ca2+ concentration increased DSI, and varying the DSI-inducing voltage step showed that the voltage dependence of DSI was like that of high-voltage-activated Ca2+ channels. 3. The P- and Q-type Ca2+ channel blocker omega-agatoxin TK (200 nM and 1 microM) and the R- and T-type Ca2+ channel blocker Ni2+ (100 microM) reduced IPSCs without reducing DSI. 4. The specific N-type Ca2+ channel antagonist omega-conotoxin GVIA (250 nM) reduced IPSC amplitudes and almost completely abolished DSI. 5. Blocking L-type Ca2+ channels with nifedipine (10 microM) had no effect on IPSCs or DSI induced by our standard protocol, but reduced DSI induced by the unclamped Na+- and Ca2+-dependent spikes that occurred when 2(triethylamino)-N-(2,6-dimethylphenyl)acetamide (QX-314) was omitted from the recording pipette solution. 6. Although intracellular Ca2+ stores were not measured, DSI was not affected by cyclopiazonic acid (CPA, 20-40 microM), a blocker of Ca2+ uptake into intracellular stores. 7. We conclude that DSI is initiated by Ca2+ influx through N- and, under certain conditions, L-type Ca2+ channels.
PubMed: 9729617
Affiliations:
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Le document en format XML
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type="wicri:source">PubMed</idno><date when="1998">1998</date><idno type="RBID">pubmed:9729617</idno><idno type="pmid">9729617</idno><idno type="wicri:Area/PubMed/Corpus">000136</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000136</idno><idno type="wicri:Area/PubMed/Curation">000136</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000136</idno><idno type="wicri:Area/PubMed/Checkpoint">000136</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000136</idno><idno type="wicri:Area/Ncbi/Merge">000176</idno><idno type="wicri:Area/Ncbi/Curation">000176</idno><idno type="wicri:Area/Ncbi/Checkpoint">000176</idno><idno type="wicri:doubleKey">0022-3751:1998:Lenz R:n:and:l</idno><idno type="wicri:Area/Main/Merge">000D16</idno><idno type="wicri:Area/Main/Curation">000C76</idno><idno type="wicri:Area/Main/Exploration">000C76</idno></publicationStmt><sourceDesc><biblStruct><analytic><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><affiliation wicri:level="2"><nlm:affiliation>Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></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><imprint><date when="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Calcium (metabolism)</term><term>Calcium Channel Blockers (pharmacology)</term><term>Calcium Channels (drug effects)</term><term>Calcium Channels (physiology)</term><term>Calcium Channels, L-Type</term><term>Evoked Potentials (drug effects)</term><term>Evoked Potentials (physiology)</term><term>Hippocampus (physiology)</term><term>In Vitro Techniques</term><term>Indoles (pharmacology)</term><term>Lidocaine (analogs & derivatives)</term><term>Lidocaine (pharmacology)</term><term>Male</term><term>Nickel (pharmacology)</term><term>Nifedipine (pharmacology)</term><term>Peptides (pharmacology)</term><term>Pyramidal Cells (drug effects)</term><term>Pyramidal Cells (physiology)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>omega-Conotoxin GVIA</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Lidocaine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Calcium Channels</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Calcium</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Calcium Channel Blockers</term><term>Indoles</term><term>Lidocaine</term><term>Nickel</term><term>Nifedipine</term><term>Peptides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Calcium Channels</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Evoked Potentials</term><term>Pyramidal Cells</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Evoked Potentials</term><term>Hippocampus</term><term>Pyramidal Cells</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Calcium Channels, L-Type</term><term>In Vitro Techniques</term><term>Male</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>omega-Conotoxin GVIA</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">1. 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 GABAAergic IPSCs lasting for approximately 1 min, was induced by depolarizing the pyramidal cell to -10 or 0 mV for 1 or 2 s. 2. Raising extracellular Ca2+ concentration increased DSI, and varying the DSI-inducing voltage step showed that the voltage dependence of DSI was like that of high-voltage-activated Ca2+ channels. 3. The P- and Q-type Ca2+ channel blocker omega-agatoxin TK (200 nM and 1 microM) and the R- and T-type Ca2+ channel blocker Ni2+ (100 microM) reduced IPSCs without reducing DSI. 4. The specific N-type Ca2+ channel antagonist omega-conotoxin GVIA (250 nM) reduced IPSC amplitudes and almost completely abolished DSI. 5. Blocking L-type Ca2+ channels with nifedipine (10 microM) had no effect on IPSCs or DSI induced by our standard protocol, but reduced DSI induced by the unclamped Na+- and Ca2+-dependent spikes that occurred when 2(triethylamino)-N-(2,6-dimethylphenyl)acetamide (QX-314) was omitted from the recording pipette solution. 6. Although intracellular Ca2+ stores were not measured, DSI was not affected by cyclopiazonic acid (CPA, 20-40 microM), a blocker of Ca2+ uptake into intracellular stores. 7. We conclude that DSI is initiated by Ca2+ influx through N- and, under certain conditions, L-type Ca2+ channels.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><noCountry><name sortKey="Alger, B E" sort="Alger, B E" uniqKey="Alger B" first="B E" last="Alger">B E Alger</name><name sortKey="Wagner, J J" sort="Wagner, J J" uniqKey="Wagner J" first="J J" last="Wagner">J J Wagner</name></noCountry><country name="États-Unis"><region name="Maryland"><name sortKey="Lenz, R A" sort="Lenz, R A" uniqKey="Lenz R" first="R A" last="Lenz">R A Lenz</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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