Synaptic excitation may activate a calcium-dependent potassium conductance in hippocampal pyramidal cells.
Identifieur interne : 000088 ( PubMed/Corpus ); précédent : 000087; suivant : 000089Synaptic excitation may activate a calcium-dependent potassium conductance in hippocampal pyramidal cells.
Auteurs : R A Nicoll ; B E AlgerSource :
- Science (New York, N.Y.) [ 0036-8075 ] ; 1981.
English descriptors
- KwdEn :
- Animals, Bicuculline (pharmacology), Calcium (pharmacology), Electric Conductivity, Electric Stimulation, Glutamates (pharmacology), Hippocampus (physiology), In Vitro Techniques, Membrane Potentials (drug effects), Neural Inhibition (drug effects), Potassium (physiology), Pyramidal Tracts (physiology), Rats, Synaptic Transmission.
- MESH :
- chemical , pharmacology : Bicuculline, Calcium, Glutamates.
- drug effects : Membrane Potentials, Neural Inhibition.
- physiology : Hippocampus, Potassium, Pyramidal Tracts.
- Animals, Electric Conductivity, Electric Stimulation, In Vitro Techniques, Rats, Synaptic Transmission.
Abstract
In hippocampal CAl pyramidal cells, orthodromic synaptic excitation is followed by an early hyperpolarization mediated by gamma-aminobutyric acid (GABA) and a late non-GABA-mediated hyperpolarization that has properties consistent with an increase in potassium conductance. Depolarizations produced by iontophoretically applied glutamate are followed by hyperpolarizations that have features in accordance with an increase in potassium conductance. The hyperpolarizations are independent of chloride and resistant to tetradotoxin but are blocked by a low-calcium, high-cobalt medium. Voltage clamping the glutamate depolarization does not reduce the subsequent hyperpolarization, indicating that the hyperpolarization results from a direct increase in calcium conductance produced by glutamate, rather than from activation of voltage-sensitive calcium channels. A single transmitter, possibly acting on one type of receptor and channel, may initiate both excitation and inhibition in the same postsynaptic cell.
PubMed: 6262912
Links to Exploration step
pubmed:6262912Le document en format XML
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Depolarizations produced by iontophoretically applied glutamate are followed by hyperpolarizations that have features in accordance with an increase in potassium conductance. The hyperpolarizations are independent of chloride and resistant to tetradotoxin but are blocked by a low-calcium, high-cobalt medium. Voltage clamping the glutamate depolarization does not reduce the subsequent hyperpolarization, indicating that the hyperpolarization results from a direct increase in calcium conductance produced by glutamate, rather than from activation of voltage-sensitive calcium channels. A single transmitter, possibly acting on one type of receptor and channel, may initiate both excitation and inhibition in the same postsynaptic cell.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">6262912</PMID><DateCreated><Year>1981</Year><Month>7</Month><Day>20</Day></DateCreated><DateCompleted><Year>1981</Year><Month>07</Month><Day>20</Day></DateCompleted><DateRevised><Year>2014</Year><Month>11</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0036-8075</ISSN><JournalIssue CitedMedium="Print"><Volume>212</Volume><Issue>4497</Issue><PubDate><Year>1981</Year><Month>May</Month><Day>22</Day></PubDate></JournalIssue><Title>Science (New York, N.Y.)</Title><ISOAbbreviation>Science</ISOAbbreviation></Journal><ArticleTitle>Synaptic excitation may activate a calcium-dependent potassium conductance in hippocampal pyramidal cells.</ArticleTitle><Pagination><MedlinePgn>957-9</MedlinePgn></Pagination><Abstract><AbstractText>In hippocampal CAl pyramidal cells, orthodromic synaptic excitation is followed by an early hyperpolarization mediated by gamma-aminobutyric acid (GABA) and a late non-GABA-mediated hyperpolarization that has properties consistent with an increase in potassium conductance. Depolarizations produced by iontophoretically applied glutamate are followed by hyperpolarizations that have features in accordance with an increase in potassium conductance. The hyperpolarizations are independent of chloride and resistant to tetradotoxin but are blocked by a low-calcium, high-cobalt medium. Voltage clamping the glutamate depolarization does not reduce the subsequent hyperpolarization, indicating that the hyperpolarization results from a direct increase in calcium conductance produced by glutamate, rather than from activation of voltage-sensitive calcium channels. A single transmitter, possibly acting on one type of receptor and channel, may initiate both excitation and inhibition in the same postsynaptic cell.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nicoll</LastName><ForeName>R A</ForeName><Initials>RA</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>NS 15764</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS-00287</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS07067</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>United States</Country><MedlineTA>Science</MedlineTA><NlmUniqueID>0404511</NlmUniqueID><ISSNLinking>0036-8075</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005971">Glutamates</NameOfSubstance></Chemical><Chemical><RegistryNumber>RWP5GA015D</RegistryNumber><NameOfSubstance UI="D011188">Potassium</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical><Chemical><RegistryNumber>Y37615DVKC</RegistryNumber><NameOfSubstance UI="D001640">Bicuculline</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001640" MajorTopicYN="N">Bicuculline</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="N">Calcium</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004553" MajorTopicYN="N">Electric Conductivity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004558" MajorTopicYN="N">Electric Stimulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005971" MajorTopicYN="N">Glutamates</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006624" MajorTopicYN="N">Hippocampus</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D066298" MajorTopicYN="N">In Vitro Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008564" MajorTopicYN="N">Membrane Potentials</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009433" MajorTopicYN="N">Neural Inhibition</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011188" MajorTopicYN="N">Potassium</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011712" MajorTopicYN="N">Pyramidal Tracts</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009435" MajorTopicYN="Y">Synaptic Transmission</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1981</Year><Month>5</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1981</Year><Month>5</Month><Day>22</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1981</Year><Month>5</Month><Day>22</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">6262912</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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