Drugs that prevent mouse sleep also block light-induced locomotor suppression, circadian rhythm phase shifts and the drop in core temperature

Abstract

Exposure of mice to a brief light stimulus during their nocturnal active phase induces several simultaneous behavioral or physiological responses, including circadian rhythm phase shifts, a drop in core body temperature (Tc), suppression of locomotor activity and sleep. Each response is triggered by light, endures for a relatively fixed interval and does not require additional light for expression. The present studies address the ability of the psychostimulant drugs, methamphetamine (MA), modafinil (MOD) or caffeine (CAF), to modify the light-induced responses. Drug or vehicle (VEH) was injected at CT11 into constant dark-housed mice then exposed to 5 min 100 μW/cm2 light or no light at CT13. Controls (VEH/Light) showed approximately 60 min phase delays. In contrast, response was substantially attenuated by each drug (only 12-15 min delays). Under a LD12:12 photoperiod, VEH/light-treated mice experienced a Tc drop of about 1.3 °C coincident with locomotor suppression and both effects were abolished by drug pretreatment. Each drug elevated activity during the post-injection interval, but there was also evidence for CAF-induced hypoactivity in the dark prior to the photic test stimulus. CAF acutely elevated Tc; MA acutely lowered it, but both drugs reduced Tc during the early dark (ZT12.5-ZT13). The ability of the psychostimulant drugs to block the several effects of light exposure is not the result of drug-induced hyperactivity. The results raise questions concerning the manner in which drugs, activity, sleep and Tc influence behavioral and physiological responses to light.

Caffeine increases light responsiveness of the mouse circadian pacemaker

“…It has been shown previously that application of an adenosine agonist attenuates the light‐induced phase delays in behaviour, which are restored by an adenosine receptor antagonist (Elliott et al ., ; Sigworth & Rea, ). In contrast, a recent study showed that caffeine administration blocks light‐induced phase delays; however, the dose applied was three times larger, and the activity of the animals was very much reduced under these conditions (Vivanco et al ., ). We found that at the level of the SCN, caffeine restored light responses.…”

Effects of lactic acid bacteria-containing foods on the quality of sleep: a placebo-controlled, double-blinded, randomized crossover study

“…Deep body temperature increased in the day and decreased in the night, while peripheral cutaneous temperature was elevated in the night. These diurnal changes in body temperature are reportedly necessary for balanced heat production and heat dissipation in the body and are deeply involved in the emergence of REM/non-REM sleep [25,26]. As a possible link between this phenomenon and the mechanism of sleeping, peroxisome proliferator-activated receptor alpha (PPARα) agonists and other drugs that accelerate lipid metabolism have been reported to be involved in the regulation of the biological clock and improvement of the circadian rhythm in sleep disorders [27].…”

Modification of 5-methoxy-N,N-dimethyltryptamine-induced hyperactivity by monoamine oxidase A inhibitor harmaline in mice and the underlying serotonergic mechanisms

“…The biphasic effects of a higher dose of harmaline (15 mg/kg) on home-cage or locomotor activity revealed in mice (Figures 1 and 4) using the automated Telemetry system [38–40] is consistent with the very recent findings on biphasic effects of harmaline on mobility (locomotor activity) obtained from rats using fully automated Force Plate Actimeters [41]. However, different from a partial attenuation of the late-phase hyperactivity by Lu AF21934, a positive allosteric modulator of metabotropic glutamate receptor 4 (mGlu4) [41], the present study showed a complete attenuation of the early-phase hypoactivity by 5-HT 1A receptor antagonist WAY-100635 (Figure 4).…”