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  <identifier identifierType="DOI">10.18453/rosdok_id00001312</identifier>
  <creators>
    <creator>
      <creatorName nameType="Personal">Badel, Gulshat</creatorName>
      <givenName>Gulshat</givenName>
      <familyName>Badel</familyName>
      <nameIdentifier nameIdentifierScheme="GND" schemeURI="http://d-nb.info/gnd/">http://d-nb.info/gnd/1048733793</nameIdentifier>
    </creator>
  </creators>
  <titles>
    <title>Role of HCN Channels in Regulation of Synaptic Plasticity at Early Postnatal Medial Perforant Path</title>
    <title>Die Rolle der HCN-Kanäle bei der Regulation der synaptischen Plastizität des postnatalen medialen Tractus perforans</title>
  </titles>
  <publisher>Universität Rostock</publisher>
  <publicationYear>2014</publicationYear>
  <resourceType resourceTypeGeneral="Text" />
  <subjects>
    <subject xml:lang="en" schemeURI="http://dewey.info/" subjectScheme="dewey">610 Medical sciences Medicine</subject>
  </subjects>
  <dates>
    <date dateType="Created">2014</date>
  </dates>
  <language>en</language>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="PURL">http://purl.uni-rostock.de/rosdok/id00001312</alternateIdentifier>
    <alternateIdentifier alternateIdentifierType="URN">urn:nbn:de:gbv:28-diss2014-0064-2</alternateIdentifier>
  </alternateIdentifiers>
  <descriptions>
    <description descriptionType="Abstract">HCN channel blocker ZD7288 depressed synaptic transmission at medial perforant path (MPP) synapses. Low-frequency stimulation (LFS) delivered to these fibers resulted in enhanced LTD after ZD7288 in P9-15 rats, but not in P30-60 rats. Hence, HCN channel activation during neuronal activity may compromise the propensity of LTD at these synapses. Results obtained with L-NAME iterated the effect of HCN channel inhibition on LTD, suggesting that retrograde signaling with NO might play a major role in the linkage between postsynaptic NMDAR activation and presynaptic HCN channel function.</description>
  </descriptions>
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