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@ARTICLE{Kanyshkova:5103,
      author       = {Kanyshkova, T. and Pawlowski, M. and Meuth, P. and Dube, C.
                      and Bender, R. A. and Brewster, A. L.. and Baumann, A. and
                      Baram, T. Z. and Pape, H.-C. and Budde, T.},
      title        = {{P}ostnatal expression pattern of {HCN} channel isoforms in
                      thalamic neurons: {R}elationship to maturation of
                      thalamocortical oscillations},
      journal      = {The journal of neuroscience},
      volume       = {29},
      issn         = {0270-6474},
      address      = {Washington, DC},
      publisher    = {Soc.},
      reportid     = {PreJuSER-5103},
      pages        = {8857 - 8847},
      year         = {2009},
      note         = {This work was supported by Deutsche Forschungsgemeinschaft
                      Grants BU 1019/8-1 and BE 4107/2-1, Interdisziplinares
                      Zentrum fur Klinische Forschung Grant Bud/005/07, and
                      National Institutes of Health Grants NS 35439 and NS 45540.
                      This work was done in partial fulfillment of the MD thesis
                      of M. P. and the PhD thesis of P. M. We thank A. Markovic,
                      E. Nass, and S. Ruppel for excellent technical assistance.},
      abstract     = {Hyperpolarization-activated cyclic nucleotide-gated cation
                      (HCN) channels are the molecular substrate of the
                      hyperpolarization-activated inward current (I(h)). Because
                      the developmental profile of HCN channels in the thalamus is
                      not well understood, we combined electrophysiological,
                      molecular, immunohistochemical, EEG recordings in vivo, and
                      computer modeling techniques to examine HCN gene expression
                      and I(h) properties in rat thalamocortical relay (TC)
                      neurons in the dorsal part of the lateral geniculate nucleus
                      and the functional consequence of this maturation.
                      Recordings of TC neurons revealed an approximate sixfold
                      increase in I(h) density between postnatal day 3 (P3) and
                      P106, which was accompanied by significantly altered current
                      kinetics, cAMP sensitivity, and steady-state activation
                      properties. Quantification on tissue levels revealed a
                      significant developmental decrease in cAMP. Consequently the
                      block of basal adenylyl cyclase activity was accompanied by
                      a hyperpolarizing shift of the I(h) activation curve in
                      young but not adult rats. Quantitative analyses of HCN
                      channel isoforms revealed a steady increase of mRNA and
                      protein expression levels of HCN1, HCN2, and HCN4 with
                      reduced relative abundance of HCN4. Computer modeling in a
                      simplified thalamic network indicated that the occurrence of
                      rhythmic delta activity, which was present in the EEG at
                      P12, differentially depended on I(h) conductance and
                      modulation by cAMP at different developmental states. These
                      data indicate that the developmental increase in I(h)
                      density results from increased expression of three HCN
                      channel isoforms and that isoform composition and
                      intracellular cAMP levels interact in determining I(h)
                      properties to enable progressive maturation of rhythmic
                      slow-wave sleep activity patterns.},
      keywords     = {Animals / Animals, Newborn / Biological Clocks: physiology
                      / Cerebral Cortex: growth $\&$ development / Cerebral
                      Cortex: metabolism / Cyclic Nucleotide-Gated Cation
                      Channels: biosynthesis / Cyclic Nucleotide-Gated Cation
                      Channels: genetics / Gene Expression Regulation,
                      Developmental: physiology / Ion Channels: biosynthesis / Ion
                      Channels: genetics / Neural Pathways: growth $\&$
                      development / Neural Pathways: metabolism / Neurons:
                      metabolism / Neurons: physiology / Potassium Channels:
                      biosynthesis / Potassium Channels: genetics / Protein
                      Isoforms: biosynthesis / Rats / Rats, Sprague-Dawley /
                      Thalamus: growth $\&$ development / Thalamus: metabolism /
                      Cyclic Nucleotide-Gated Cation Channels (NLM Chemicals) /
                      HCN2 potassium channel (NLM Chemicals) / HCN3 protein, rat
                      (NLM Chemicals) / HCN4 protein, rat (NLM Chemicals) / Ion
                      Channels (NLM Chemicals) / Potassium Channels (NLM
                      Chemicals) / Protein Isoforms (NLM Chemicals) /
                      hyperpolarization-activated cation channel (NLM Chemicals) /
                      J (WoSType)},
      cin          = {ISB-1},
      ddc          = {590},
      cid          = {I:(DE-Juel1)VDB922},
      pnm          = {Programm Biosoft},
      pid          = {G:(DE-Juel1)FUEK443},
      shelfmark    = {Neurosciences},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:19587292},
      pmc          = {pmc:PMC2768285},
      UT           = {WOS:000267818400026},
      doi          = {10.1523/JNEUROSCI.0689-09.2009},
      url          = {https://juser.fz-juelich.de/record/5103},
}