Skip to main content
. 2010 May 5;30(18):6302–6314. doi: 10.1523/JNEUROSCI.5482-09.2010

Figure 3.

Figure 3.

Disruption of mTOR signaling attenuates light-induced phase delaying of circadian locomotor activity. A, B, Representative double-plotted actographs of wheel-running activity. Initially, mice were entrained on a 12 h LD cycle and then transferred to total darkness. After ∼10 d under DD, mice were infused with DMSO vehicle (A) or the mTOR inhibitor rapamycin (100 μm; B) 30 min before light exposure (100 lux, 15 min) at CT15 (red asterisks). Animals free ran for 14 d and then received a second infusion of rapamycin (A) or DMSO (B) followed by light treatment. Regression lines approximate the phase-delaying effects of light. The small horizontal red bars in the activity records denote an “off-line” period when wheel-running activity was not recorded. C, Representative actograph shows that rapamycin (100 μm) infusion at CT15 did not markedly affect clock timing or phasing. D, Statistical representation of the early-night phase-shifting data. Of note, the light-evoked phase delay was significantly attenuated by rapamycin. Numbers above the bars denote the number of animals examined for each condition. E, Light-evoked p70 S6K phosphorylation. To test whether the light intensity (100 lux, 15 min) used in the behavioral experiments evokes mTOR activation, mice were exposed to light (100 lux, 15 min) at CT22 and killed immediately thereafter. Immunohistochemical labeling revealed a light-evoked increase in p-p70 S6K, relative to control mice (no light). Scale bar, 100 μm.