1 Ocak 2015 Dergi makalesi Açık Erişim

Lenkey, Nora; Kirizs, Tekla; Holderith, Noemi; Mate, Zoltan; Szabo, Gabor; Vizi, E. Sylvester; Hajos, Norbert; Nusser, Zoltan

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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/81947</identifier>
  <creators>
    <creator>
      <creatorName>Lenkey, Nora</creatorName>
      <givenName>Nora</givenName>
      <familyName>Lenkey</familyName>
      <affiliation>Hungarian Acad Sci, Inst Expt Med, Lendulet Lab Cellular Neurophysiol, H-1083 Budapest, Hungary</affiliation>
    </creator>
    <creator>
      <creatorName>Kirizs, Tekla</creatorName>
      <givenName>Tekla</givenName>
      <familyName>Kirizs</familyName>
    </creator>
    <creator>
      <creatorName>Holderith, Noemi</creatorName>
      <givenName>Noemi</givenName>
      <familyName>Holderith</familyName>
      <affiliation>Hungarian Acad Sci, Inst Expt Med, Lendulet Lab Cellular Neurophysiol, H-1083 Budapest, Hungary</affiliation>
    </creator>
    <creator>
      <creatorName>Mate, Zoltan</creatorName>
      <givenName>Zoltan</givenName>
      <familyName>Mate</familyName>
      <affiliation>Hungarian Acad Sci, Inst Expt Med, Div Med Gene Technol, H-1083 Budapest, Hungary</affiliation>
    </creator>
    <creator>
      <creatorName>Szabo, Gabor</creatorName>
      <givenName>Gabor</givenName>
      <familyName>Szabo</familyName>
      <affiliation>Hungarian Acad Sci, Inst Expt Med, Div Med Gene Technol, H-1083 Budapest, Hungary</affiliation>
    </creator>
    <creator>
      <creatorName>Vizi, E. Sylvester</creatorName>
      <givenName>E. Sylvester</givenName>
      <familyName>Vizi</familyName>
      <affiliation>Hungarian Acad Sci, Inst Expt Med, Lab Drug Res, H-1083 Budapest, Hungary</affiliation>
    </creator>
    <creator>
      <creatorName>Hajos, Norbert</creatorName>
      <givenName>Norbert</givenName>
      <familyName>Hajos</familyName>
      <affiliation>Hungarian Acad Sci, Inst Expt Med, Lendulet Lab Network Neurophysiol, H-1083 Budapest, Hungary</affiliation>
    </creator>
    <creator>
      <creatorName>Nusser, Zoltan</creatorName>
      <givenName>Zoltan</givenName>
      <familyName>Nusser</familyName>
      <affiliation>Hungarian Acad Sci, Inst Expt Med, Lendulet Lab Cellular Neurophysiol, H-1083 Budapest, Hungary</affiliation>
    </creator>
  </creators>
  <titles>
    <title>Tonic Endocannabinoid-Mediated Modulation Of Gaba Release Is Independent Of The Cb1 Content Of Axon Terminals</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2015</publicationYear>
  <dates>
    <date dateType="Issued">2015-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/81947</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1038/ncomms7557</relatedIdentifier>
  </relatedIdentifiers>
  <rightsList>
    <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
  </rightsList>
  <descriptions>
    <description descriptionType="Abstract">The release of GABA from cholecystokinin-containing interneurons is modulated by type-1 cannabinoid receptors (CB1). Here we tested the hypothesis that the strength of CB1-mediated modulation of GABA release is related to the CB1 content of axon terminals. Basket cell boutons have on average 78% higher CB1 content than those of dendritic-layer-innervating (DLI) cells, a consequence of larger bouton surface and higher CB1 density. The CB1 antagonist AM251 caused a 54% increase in action potential-evoked [Ca2+] in boutons of basket cells, but not in DLI cells. However, the effect of AM251 did not correlate with CB1 immunoreactivity of individual boutons. Moreover, a CB1 agonist decreased [Ca2+] in a cell type-and CB1-content-independent manner. Replica immunogold labelling demonstrated the colocalization of CB1 with the Cav2.2 Ca2+ channel subunit. Our data suggest that only a subpopulation of CB(1)s, within nanometre distances from their target Cav2.2 channels, are responsible for endocannabinoid-mediated modulation of GABA release.</description>
  </descriptions>
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