% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Knop:1483,
      author       = {Knop, G.C. and Seeliger, M.W. and Thiel, F. and Mataruga,
                      A. and Kaupp, U. B. and Friedburg, C. and Tanimoto, N. and
                      Müller, F.},
      title        = {{L}ight responses in the mouse retina are prolonged upon
                      targeted deletion of the {HCN}1 channel gene},
      journal      = {European journal of neuroscience},
      volume       = {28},
      issn         = {0953-816X},
      address      = {Oxford [u.a.]},
      publisher    = {Blackwell},
      reportid     = {PreJuSER-1483},
      pages        = {2221 - 2230},
      year         = {2008},
      note         = {We thank Dr Eric Kandel ( Columbia University, USA) for
                      providing the HCN1 knock-out line, Christoph Aretzweiler for
                      technical assistance in immunohistochemistry and genotyping
                      of HCN1 knock-out animals, Mechthilde Bruns for help in cell
                      culture, and Dr Wolfgang Bonigk for the cDNA of murine HCN1.
                      M. W. Seeliger was supported by the Deutsche
                      Forschungsgemeinschaft ( DFG Se837/4-1 and Se837/5-1).},
      abstract     = {Hyperpolarization-activated and cyclic nucleotide-gated
                      (HCN) channels contribute to pacemaker activity, and
                      co-determine the integrative behaviour of neurons and shape
                      their response to synaptic stimulation. Four channel
                      isoforms, HCN1-4, have been described in mammals. Recent
                      studies showed particularly strong expression of HCN1
                      channels in rods and cones of the rat retina, suggesting
                      that HCN1 channels are involved in the shaping of light
                      responses in both types of photoreceptors. Therefore, the
                      loss of HCN1 channels should lead to pronounced changes in
                      light-induced electrical responses under both scotopic and
                      photopic conditions. This was tested using a mouse
                      transgenic approach. We used immunohistochemistry and
                      patch-clamp recording to study the distribution of HCN1
                      channels in the mouse retina. HCN1 channels were strongly
                      expressed in rod and cone photoreceptors, as well as in some
                      bipolar, amacrine and ganglion cell types. In
                      electroretinograms (ERGs) from animals in which the HCN1
                      channel gene had been knocked out, the b-wave amplitudes
                      were unaltered (scotopic conditions) or somewhat reduced
                      (photopic conditions), whereas the duration of both scotopic
                      and photopic ERG responses was strikingly prolonged. Our
                      data suggest that in visual information processing,
                      shortening and shaping of light responses by activation of
                      HCN1 at the level of the photoreceptors is an important step
                      in both scotopic and photopic pathways.},
      keywords     = {Amacrine Cells: metabolism / Amacrine Cells: radiation
                      effects / Animals / Cyclic Nucleotide-Gated Cation Channels:
                      genetics / Electroretinography / Immunohistochemistry /
                      Membrane Potentials: genetics / Membrane Potentials:
                      radiation effects / Mice / Mice, Inbred C57BL / Mice,
                      Knockout / Neurons: metabolism / Neurons: radiation effects
                      / Organ Culture Techniques / Patch-Clamp Techniques / Photic
                      Stimulation / Photoreceptor Cells, Vertebrate: metabolism /
                      Photoreceptor Cells, Vertebrate: radiation effects /
                      Potassium Channels: genetics / Retina: metabolism / Retina:
                      radiation effects / Retinal Bipolar Cells: metabolism /
                      Retinal Bipolar Cells: radiation effects / Retinal Ganglion
                      Cells: metabolism / Retinal Ganglion Cells: radiation
                      effects / Synaptic Transmission: genetics / Synaptic
                      Transmission: radiation effects / Vision, Ocular: genetics /
                      Cyclic Nucleotide-Gated Cation Channels (NLM Chemicals) /
                      Potassium Channels (NLM Chemicals) /
                      hyperpolarization-activated cation channel (NLM Chemicals) /
                      J (WoSType)},
      cin          = {INB-1},
      ddc          = {610},
      cid          = {I:(DE-Juel1)VDB804},
      pnm          = {Funktion und Dysfunktion des Nervensystems},
      pid          = {G:(DE-Juel1)FUEK409},
      shelfmark    = {Neurosciences},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:19019198},
      UT           = {WOS:000261184800006},
      doi          = {10.1111/j.1460-9568.2008.06512.x},
      url          = {https://juser.fz-juelich.de/record/1483},
}