% 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{Zobeiri:840568,
      author       = {Zobeiri, Mehrnoush and Chaudhary, Rahul and Datunashvili,
                      Maia and Heuermann, Robert J. and Lüttjohann, Annika and
                      Narayanan, Venu and Balfanz, Sabine and Meuth, Patrick and
                      Chetkovich, Dane M. and Pape, Hans-Christian and Baumann, A.
                      and van Luijtelaar, Gilles and Budde, Thomas},
      title        = {{M}odulation of thalamocortical oscillations by {TRIP}8b,
                      an auxiliary subunit for {HCN} channels},
      journal      = {Brain structure $\&$ function},
      volume       = {223},
      issn         = {1863-2661},
      address      = {Berlin},
      publisher    = {Springer},
      reportid     = {FZJ-2017-08073},
      pages        = {1537-1564},
      year         = {2018},
      abstract     = {Hyperpolarization-activated cyclic nucleotide-gated cation
                      (HCN) channels have important functions in controlling
                      neuronal excitability and generating rhythmic oscillatory
                      activity. The role of tetratricopeptide repeat-containing
                      Rab8b-interacting protein (TRIP8b) in regulation of
                      hyperpolarization-activated inward current, I h, in the
                      thalamocortical system and its functional relevance for the
                      physiological thalamocortical oscillations were
                      investigated. A significant decrease in I h current density,
                      in both thalamocortical relay (TC) and cortical pyramidal
                      neurons was found in TRIP8b-deficient mice (TRIP8b−/−).
                      In addition basal cAMP levels in the brain were found to be
                      decreased while the availability of the fast transient
                      A-type K+ current, I A, in TC neurons was increased. These
                      changes were associated with alterations in intrinsic
                      properties and firing patterns of TC neurons, as well as
                      intrathalamic and thalamocortical network oscillations,
                      revealing a significant increase in slow oscillations in the
                      delta frequency range (0.5–4 Hz) during episodes of
                      active-wakefulness. In addition, absence of TRIP8b
                      suppresses the normal desynchronization response of the EEG
                      during the switch from slow-wave sleep to wakefulness. It is
                      concluded that TRIP8b is necessary for the modulation of
                      physiological thalamocortical oscillations due to its direct
                      effect on HCN channel expression in thalamus and cortex and
                      that mechanisms related to reduced cAMP signaling may
                      contribute to the present findings.},
      cin          = {ICS-4},
      ddc          = {610},
      cid          = {I:(DE-Juel1)ICS-4-20110106},
      pnm          = {552 - Engineering Cell Function (POF3-552)},
      pid          = {G:(DE-HGF)POF3-552},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29168010},
      UT           = {WOS:000428419500029},
      doi          = {10.1007/s00429-017-1559-z},
      url          = {https://juser.fz-juelich.de/record/840568},
}