Caffeine increases light responsiveness of the mouse circadian pacemaker

Sep 9, 2014The European journal of neuroscience

Caffeine makes the mouse body clock more sensitive to light

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Abstract

Caffeine restores light responsiveness of the suprachiasmatic nucleus (SCN) after 6 hours of sleep deprivation in mice.

Sleep deprivation is associated with reduced neuronal activity in the SCN, which is crucial for regulating circadian rhythms.
After 6 hours of sleep deprivation, the SCN's sustained response to light is significantly diminished.
Caffeine administration can restore the SCN's responsiveness to light following sleep deprivation.
Chronic caffeine treatment in constant light conditions leads to enhanced period lengthening in mice.
Increased pressure for sleep may alter the functioning of the circadian pacemaker by affecting SCN sensitivity to light.

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Caffeine is the most commonly used psychoactive stimulant worldwide. It reduces sleep and sleepiness by blocking access to the adenosine receptor. The level of adenosine increases during sleep deprivation, and is thought to induce sleepiness and initiate sleep. Light-induced phase shifts of the rest-activity circadian rhythms are mediated by light-responsive neurons of the suprachiasmatic nucleus (SCN) of the hypothalamus, where the circadian clock of mammals resides. Previous studies have shown that sleep deprivation reduces circadian clock phase-shifting capacity and decreases SCN neuronal activity. In addition, application of adenosine agonists and antagonists mimics and blocks, respectively, the effect of sleep deprivation on light-induced phase shifts in behaviour, suggesting a role for adenosine. In the present study, we examined the role of sleep deprivation in and the effect of caffeine on light responsiveness of the SCN. We performed in vivo electrical activity recordings of the SCN in freely moving mice, and showed that the sustained response to light of SCN neuronal activity was attenuated after 6 h of sleep deprivation prior to light exposure. Subsequent intraperitoneal application of caffeine was able to restore the response to light. Finally, we performed behavioural recordings in constant conditions, and found enhanced period lengthening during chronic treatment with caffeine in drinking water in constant light conditions. The data suggest that increased homeostatic sleep pressure changes circadian pacemaker functioning by reducing SCN neuronal responsiveness to light. The electrophysiological and behavioural data together provide evidence that caffeine enhances clock sensitivity to light.

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Caffeine increases light responsiveness of the mouse circadian pacemaker

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