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@ARTICLE{Korkmaz:1040329,
      author       = {Korkmaz, Hüseyin and Anstötz, Max and Wellinghof, Tim and
                      Fazari, Benedetta and Hallenberger, Angelika and Bergmann,
                      Ann Kathrin and Niggetiedt, Elena and Güven, Fatma Delâl
                      and Tundo-Lavalle, Federica and Purath, Fathima Faiba A. and
                      Bochinsky, Kevin and Gremer, Lothar and Willbold, Dieter and
                      von Gall, Charlotte and Ali, Amira A. H.},
      title        = {{L}oss of {B}mal1 impairs the glutamatergic light input to
                      the {SCN} in mice},
      journal      = {Frontiers in cellular neuroscience},
      volume       = {19},
      issn         = {1662-5102},
      address      = {Lausanne},
      publisher    = {Frontiers Research Foundation},
      reportid     = {FZJ-2025-01842},
      pages        = {1538985},
      year         = {2025},
      abstract     = {Introduction: Glutamate represents the dominant
                      neurotransmitter that conveys the light information to the
                      brain, including the suprachiasmatic nucleus (SCN), the
                      central pacemaker for the circadian system. The neuronal and
                      astrocytic glutamate transporters are crucial for
                      maintaining efficient glutamatergic signaling. In the SCN,
                      glutamatergic nerve terminals from the retina terminate on
                      vasoactive intestinal polypeptide (VIP) neurons, which are
                      essential for circadian functions. To date, little is known
                      about the role of the core circadian clock gene, Bmal1, in
                      glutamatergic neurotransmission of light signal to various
                      brain regions.Methods: The aim of this study was to further
                      elucidate the role of Bmal1 in glutamatergic
                      neurotransmission from the retina to the SCN. We therefore
                      examined the spontaneous rhythmic locomotor activity,
                      neuronal and glial glutamate transporters, as well as the
                      ultrastructure of the synapse between the retinal ganglion
                      cells (RGCs) and the SCN in adult male Bmal1−/−
                      mice.Results: We found that the deletion of Bmal1 affects
                      the light-mediated behavior in mice, decreases the retinal
                      thickness and affects the vesicular glutamate transporters
                      (vGLUT1, 2) in the retina. Within the SCN, the
                      immunoreaction of vGLUT1, 2, glial glutamate transporters
                      (GLAST) and VIP was decreased while the glutamate
                      concentration was elevated. At the ultrastructure level, the
                      presynaptic terminals were enlarged and the distance between
                      the synaptic vesicles and the synaptic cleft was increased,
                      indicative of a decrease in the readily releasable pool at
                      the excitatory synapses in Bmal1−/−.Conclusion: Our data
                      suggests that Bmal1 deletion affects the glutamate
                      transmission in the retina and the SCN and affects the
                      behavioral responses to light.},
      cin          = {IBI-7},
      ddc          = {610},
      cid          = {I:(DE-Juel1)IBI-7-20200312},
      pnm          = {5244 - Information Processing in Neuronal Networks
                      (POF4-524)},
      pid          = {G:(DE-HGF)POF4-5244},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {40083633},
      UT           = {WOS:001445118900001},
      doi          = {10.3389/fncel.2025.1538985},
      url          = {https://juser.fz-juelich.de/record/1040329},
}