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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},
}