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. 2021 Jan 20;41(3):502–512. doi: 10.1523/JNEUROSCI.2015-20.2020

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Copyright © 2021 Hamnett et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Figure 5. — Deletion of BMAL1 from VPAC2-Cre-expressing cells compromises SCN molecular pace-making. A, Representative, baseline-corrected PER2::LUCIFERASE bioluminescence traces from control, VPAC2-Cre/Bmal1^flx/–, and Drd1a-Cre/Bmal1^flx/– SCN dissected in dim red light following recording of wheel-running rhythms in DD. B, Period (mean ± SEM) of the first 4 bioluminescent cycles recorded from adult SCN slices; genotypes as in A. n = 8 (Bmal1^WT/–), n = 7 (Bmal1^flx/–), n = 5 (VPAC2-Cre/Bmal1^WT/–), n = 11 (VPAC2-Cre/Bmal1^flx/–), and n = 6 (Drd1a-Cre/Bmal1^flx/–). C, RAE scores (mean ± SEM) for bioluminescent recordings from SCN slices. n values same as in B. D, Representative PER2::LUCIFERASE bioluminescence rhythms from VPAC2-Cre/Bmal1^flx/– SCN slices alongside respective actograms from corresponding mice. “WT-like,” “Arrhythmic,” or “Split” beside the actograms indicates the phenotypic category. **p < 0.01; ***p < 0.001; one-way ANOVA, with Tukey's post hoc test.