% 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{Datunashvili:857201,
      author       = {Datunashvili, Maia and Chaudhary, Rahul and Zobeiri,
                      Mehrnoush and Lüttjohann, Annika and Mergia, Evanthia and
                      Baumann, Arnd and Balfanz, Sabine and Budde, Björn and van
                      Luijtelaar, Gilles and Pape, Hans-Christian and Koesling,
                      Doris and Budde, Thomas},
      title        = {{M}odulation of {H}yperpolarization-{A}ctivated {I}nward
                      {C}urrent and {T}halamic {A}ctivity {M}odes by {D}ifferent
                      {C}yclic {N}ucleotides},
      journal      = {Frontiers in cellular neuroscience},
      volume       = {12},
      issn         = {1662-5102},
      address      = {Lausanne},
      publisher    = {Frontiers Research Foundation},
      reportid     = {FZJ-2018-06438},
      pages        = {369},
      year         = {2018},
      abstract     = {The hyperpolarization-activated inward current, Ih, plays a
                      key role in the generation of rhythmic activities in
                      thalamocortical (TC) relay neurons. Cyclic nucleotides, like
                      3′,5′-cyclic adenosine monophosphate (cAMP), facilitate
                      voltage-dependent activation of hyperpolarization-activated
                      cyclic nucleotide-gated (HCN) channels by shifting the
                      activation curve of Ih to more positive values and thereby
                      terminating the rhythmic burst activity. The role of
                      3′,5′-cyclic guanosine monophosphate (cGMP) in
                      modulation of Ih is not well understood. To determine the
                      possible role of the nitric oxide (NO)-sensitive
                      cGMP-forming guanylyl cyclase 2 (NO-GC2) in controlling the
                      thalamic Ih, the voltage-dependency and
                      cGMP/cAMP-sensitivity of Ih was analyzed in TC neurons of
                      the dorsal part of the lateral geniculate nucleus (dLGN) in
                      wild type (WT) and NO-GC2-deficit (NO-GC2−/−) mice.
                      Whole cell voltage clamp recordings in brain slices revealed
                      a more hyperpolarized half maximal activation (V1/2) of Ih
                      in NO-GC2−/− TC neurons compared to WT. Different
                      concentrations of 8-Br-cAMP/8-Br-cGMP induced dose-dependent
                      positive shifts of V1/2 in both strains. Treatment of WT
                      slices with lyase enzyme (adenylyl and guanylyl cyclases)
                      inhibitors (SQ22536 and ODQ) resulted in further
                      hyperpolarized V1/2. Under current clamp conditions
                      NO-GC2−/− neurons exhibited a reduction in the
                      Ih-dependent voltage sag and reduced action potential firing
                      with hyperpolarizing and depolarizing current steps,
                      respectively. Intrathalamic rhythmic bursting activity in
                      brain slices and in a simplified mathematical model of the
                      thalamic network was reduced in the absence of NO-GC2. In
                      freely behaving NO-GC2−/− mice, delta and theta band
                      activity was enhanced during active wakefulness (AW) as well
                      as rapid eye movement (REM) sleep in cortical local field
                      potential (LFP) in comparison to WT. These findings indicate
                      that cGMP facilitates Ih activation and contributes to a
                      tonic activity in TC neurons. On the network level basal
                      cGMP production supports fast rhythmic activity in the
                      cortex.},
      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:30405353},
      UT           = {WOS:000448147900001},
      doi          = {10.3389/fncel.2018.00369},
      url          = {https://juser.fz-juelich.de/record/857201},
}