N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells.
Identifieur interne : 000136 ( PubMed/Corpus ); précédent : 000135; suivant : 000137N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells.
Auteurs : R A Lenz ; 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
Links to Exploration step
pubmed:9729617Le document en format XML
<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><affiliation><nlm:affiliation>Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.</nlm:affiliation></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></titleStmt><publicationStmt><idno 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></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><nlm:affiliation>Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.</nlm:affiliation></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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9729617</PMID><DateCreated><Year>1998</Year><Month>12</Month><Day>02</Day></DateCreated><DateCompleted><Year>1998</Year><Month>12</Month><Day>02</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-3751</ISSN><JournalIssue CitedMedium="Print"><Volume>512 ( Pt 1)</Volume><PubDate><Year>1998</Year><Month>Oct</Month><Day>01</Day></PubDate></JournalIssue><Title>The Journal of physiology</Title><ISOAbbreviation>J. Physiol. (Lond.)</ISOAbbreviation></Journal><ArticleTitle>N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells.</ArticleTitle><Pagination><MedlinePgn>61-73</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lenz</LastName><ForeName>R A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wagner</LastName><ForeName>J J</ForeName><Initials>JJ</Initials></Author><Author ValidYN="Y"><LastName>Alger</LastName><ForeName>B E</ForeName><Initials>BE</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 NS030219</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS07375</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS30219</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS22010</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 NS007375</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Physiol</MedlineTA><NlmUniqueID>0266262</NlmUniqueID><ISSNLinking>0022-3751</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002121">Calcium Channel Blockers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015220">Calcium Channels</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020746">Calcium Channels, L-Type</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007211">Indoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010455">Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>21306-56-9</RegistryNumber><NameOfSubstance UI="C012647">QX-314</NameOfSubstance></Chemical><Chemical><RegistryNumber>7OV03QG267</RegistryNumber><NameOfSubstance UI="D009532">Nickel</NameOfSubstance></Chemical><Chemical><RegistryNumber>92078-76-7</RegistryNumber><NameOfSubstance UI="D020866">omega-Conotoxin GVIA</NameOfSubstance></Chemical><Chemical><RegistryNumber>98PI200987</RegistryNumber><NameOfSubstance UI="D008012">Lidocaine</NameOfSubstance></Chemical><Chemical><RegistryNumber>I9ZF7L6G2L</RegistryNumber><NameOfSubstance 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MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017966" MajorTopicYN="N">Pyramidal Cells</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020866" MajorTopicYN="N">omega-Conotoxin GVIA</DescriptorName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC2231194</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1998</Year><Month>9</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1998</Year><Month>9</Month><Day>8</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate 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