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. 2019 Dec 13;68(6):1131–1147. doi: 10.1002/glia.23764

Figure 2.

Figure 2

Bmal1cKO mice showed increased food intake with no alterations in the brain reward systems. (a) Daily food intake was determined in control and Bmal1cKO mice after 1, 2, 3, 6, and 12 months of TM treatment. Animals were maintained in 12 hr:12 hr light–dark cycles and fed ad libitum with a standard mouse chow. Data are represented as mean ± SEM (n = 8, paired t‐test, **p < .01 vs. control animals). (b) Activity waveforms for control (n = 8) and Bmal1cKO (n = 7) mice, 2 months after TM treatment, in 12 hr: 12 hr light–dark cycles. Activity counts are expressed as the average amount of activity in 5 min bins. Data plotted is given in ZT, such that ZT0 = lights on. The value expresses the means + SEM. (c) Food intake was determined in control and Bmal1cKO mice after 2 months of TM treatment. Animals were maintained in 12 hr:12 hr light–dark cycles and fed ad libitum with a standard mouse chow. Data are represented as mean ± SEM (n = 8, paired t‐test, *p < .05 vs. control animals). (d) Number of nose spokes performed by control and Bmal1cKO mice, 2 months after TM treatment, during fixed ratio (FR), and progressive ratio (PR) sessions in the operant conditioning test. Data are represented as mean ± SEM (n = 4 for controls and n = 11 for Bmal1cKOs). (e) Mean ± SEM breakpoints in control (n = 4) and Bmal1cKO (n = 11) mice, 2 months after TM treatment, in the operant conditioning test [Color figure can be viewed at wileyonlinelibrary.com]