Caffeine is commonly used to combat high sleep pressure on a daily basis. However, interference with sleep–wake regulation could disturb neural homeostasis and insufficient sleep could lead to alterations in human gray matter. Hence, in this double-blind, randomized, cross-over study, we examined the impact of 10-day caffeine (3 × 150 mg/day) on human gray matter volumes (GMVs) and cerebral blood flow (CBF) by fMRI MP-RAGE and arterial spin-labeling sequences in 20 habitual caffeine consumers, compared with 10-day placebo (3 × 150 mg/day). Sleep pressure was quantified by electroencephalographic slow-wave activity (SWA) in the previous nighttime sleep. Nonparametric voxel-based analyses revealed a significant reduction in GMV in the medial temporal lobe (mTL) after 10 days of caffeine intake compared with 10 days of placebo, voxel-wisely adjusted for CBF considering the decreased perfusion after caffeine intake compared with placebo. Larger GMV reductions were associated with higher individual concentrations of caffeine and paraxanthine. Sleep SWA was, however, neither different between conditions nor associated with caffeine-induced GMV reductions. Therefore, the data do not suggest a link between sleep depth during daily caffeine intake and changes in brain morphology. In conclusion, daily caffeine intake might induce neural plasticity in the mTL depending on individual metabolic processes.

Due to an oversight during manuscript preparation, the following equations were wrongly detailed within the Supplemental Information. The correct versions, which were used to generate the published data, are detailed below. This error has had no repercussions on the data as reported.(1) Vector sum magnitude and preferred orientations were derived from the average vector of responses (Swindale, 1998; Batschelet, 1981). For a set of N test orientations, x i , i = 0,1.NÀ1 which are uniformly distributed over 0-360 are determined by first calculating two components, a and b, defined byWhere Iðx i Þ is the determined integral response per epoch. The preferred orientation, q, can then be calculated asThe vector magnitude of the response is defined asNote: as epoch integrals are not all > 0, a normalized vector sum could not be used.(2) 1-Circular variance and complex angle. Circular variance defined as V = 1 À jRj (Batschelet, 1981) where R is defined byThus 1-circular variance is equal the absolute value of RðjRjÞ and the preferred angle, q, can then be calculated as q = atan2ðimagðRÞ; realðRÞÞ if a > 0 ðfrom Eq 1aÞ or q = atan2ðimagðRÞ; realðRÞÞ + pi if a < 0: ðfrom Eq 1aÞ (2b) 992 Neuron 77, 992-994, March 6, 2013 ª2013 Elsevier Inc.

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We examined whether dynamically changing light across a scheduled 16-h waking day influences sleepiness, cognitive performance, visual comfort, melatonin secretion, and sleep under controlled laboratory conditions in healthy men. Fourteen participants underwent a 49-h laboratory protocol in a repeated-measures study design. They spent the first 5 hours in the evening under standard lighting, followed by an 8-h nocturnal sleep episode at habitual bedtimes. Thereafter, volunteers either woke up to static light or to a dynamic light that changed spectrum and intensity across the scheduled 16-h waking day. Following an 8-h nocturnal sleep episode, the volunteers spent another 11 hours either under static or dynamic light. Static light attenuated the evening rise in melatonin levels more compared to dynamic light as indexed by a significant reduction in the melatonin AUC prior to bedtime during static light only. Participants felt less vigilant in the evening during dynamic light. After dynamic light, sleep latency was significantly shorter in both the baseline and treatment night while sleep structure, sleep quality, cognitive performance, and visual comfort did not significantly differ. The study shows that dynamic changes in spectrum and intensity of light promote melatonin secretion and sleep initiation in healthy men.

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