In humans, some evidence suggests that there are two different types of spindles during sleep, which differ by their scalp topography and possibly some aspects of their regulation. To test for the existence of two different spindle types, we characterized the activity associated with slow (11-13 Hz) and fast (13-15 Hz) spindles, identified as discrete events during non-rapid eye movement sleep, in non-sleepdeprived human volunteers, using simultaneous electroencephalography and functional MRI. An activation pattern common to both spindle types involved the thalami, paralimbic areas (anterior cingulate and insular cortices), and superior temporal gyri. No thalamic difference was detected in the direct comparison between slow and fast spindles although some thalamic areas were preferentially activated in relation to either spindle type. Beyond the common activation pattern, the increases in cortical activity differed significantly between the two spindle types. Slow spindles were associated with increased activity in the superior frontal gyrus. In contrast, fast spindles recruited a set of cortical regions involved in sensorimotor processing, as well as the mesial frontal cortex and hippocampus. The recruitment of partially segregated cortical networks for slow and fast spindles further supports the existence of two spindle types during human non-rapid eye movement sleep, with potentially different functional significance.H uman sleep is associated with a profound modification of consciousness and the emergence of distinct sleep oscillations. In the early stages of non-rapid eye movement (NREM) sleep, electroencephalographic recordings show characteristic spindle oscillations. In humans, spindles consist of waxing-and-waning 11-to 15-Hz oscillations, lasting 0.5-3 sec. At the cellular level, spindles are associated with substantial neuronal activity. Spindles arise from cyclic inhibition of thalamo-cortical (TC) neurons by reticular thalamic neurons. Postinihibitory rebound spike bursts in TC cells entrain cortical populations in spindle oscillations (1). These neuronal mechanisms, which involve large TC populations, are thought to shape the processing of information during light NREM sleep and participate in the alteration of consciousness that characterizes this stage of sleep.Little is known on the cerebral correlates of human spindles. Early positron emission tomography studies reported a negative relationship between thalamic cerebral blood flow and the power spectrum in the spindle frequency band (2). However, the low temporal resolution of positron emission tomography did not allow for a fine-grained characterization of the cerebral correlates of human spindles. In addition, two kinds of spindles are described in humans. Slow spindles (Ͻ13 Hz) predominate over frontal, whereas fast spindles (Ͼ13 Hz) prevail over centro-parietal areas. The difference in spindle scalp topography is also reflected by profound functional differences. These two spindling activities differ by their circadian and homeostatic regul...
Functional magnetic resonance imaging (fMRI) was used to investigate the cerebral correlates of motor sequence memory consolidation. Participants were scanned while training on an implicit oculomotor sequence learning task and during a single testing session taking place 30 min, 5 hr, or 24 hr later. During training, responses observed in hippocampus and striatum were linearly related to the gain in performance observed overnight, but not over the day. Responses in both structures were significantly larger at 24 hr than at 30 min or 5 hr. Additionally, the competitive interaction observed between these structures during training became cooperative overnight. These results stress the importance of both hippocampus and striatum in procedural memory consolidation. Responses in these areas during training seem to condition the overnight memory processing that is associated with a change in their functional interactions. These results show that both structures interact during motor sequence consolidation to optimize subsequent behavior.
Slow wave sleep (SWS) is associated with spontaneous brain oscillations that are thought to participate in sleep homeostasis and to support the processing of information related to the experiences of the previous awake period. At the cellular level, during SWS, a slow oscillation (<1 Hz) synchronizes firing patterns in large neuronal populations and is reflected on electroencephalography (EEG) recordings as large-amplitude, low-frequency waves. By using simultaneous EEG and event-related functional magnetic resonance imaging (fMRI), we characterized the transient changes in brain activity consistently associated with slow waves (>140 V) and delta waves (75-140 V) during SWS in 14 non-sleep-deprived normal human volunteers. Significant increases in activity were associated with these waves in several cortical areas, including the inferior frontal, medial prefrontal, precuneus, and posterior cingulate areas. Compared with baseline activity, slow waves are associated with significant activity in the parahippocampal gyrus, cerebellum, and brainstem, whereas delta waves are related to frontal responses. No decrease in activity was observed. This study demonstrates that SWS is not a state of brain quiescence, but rather is an active state during which brain activity is consistently synchronized to the slow oscillation in specific cerebral regions. The partial overlap between the response pattern related to SWS waves and the waking default mode network is consistent with the fascinating hypothesis that brain responses synchronized by the slow oscillation restore microwake-like activity patterns that facilitate neuronal interactions.fMRI ͉ neuroimaging ͉ sleep physiology ͉ slow oscillation D uring the deepest stage of nonrapid eye movement (NREM) sleep, also referred to as slow wave sleep (SWS) in humans (stage 3-4 of sleep), spontaneous brain activity is organized by specific physiological rhythms, the neural correlates of which have been described in animals (1). Unit recordings have shown that neuronal activity during SWS is characterized by a fundamental oscillation of membrane potential. This so-called ''slow oscillation'' (Ͻ1 Hz) is recorded in all major types of neocortical neurons during SWS and is composed of a depolarizing phase, associated with important neuronal firing (''up state''), followed by a hyperpolarizing phase during which cortical neurons remain silent for a few hundred milliseconds (''down state'') (2, 3). The slow oscillation occurs synchronously in large neuronal populations in such a way that it can be reflected on electroencephalography (EEG) recordings as large-amplitude, low-frequency waves (4).Delta rhythm (1-4 Hz) is another characteristic oscillation of NREM sleep. The neural underpinnings of delta rhythm remain uncertain, however. In the dorsal thalamus, a clock-like delta rhythm is generated by the interplay of two intrinsic membrane currents, although another delta rhythm survives complete thalamectomy, suggesting a cortical origin (1).In humans, a slow oscillation was identified on s...
After encoding, memory traces are initially fragile and have to be reinforced to become permanent. The initial steps of this process occur at a cellular level within minutes or hours. Besides this rapid synaptic consolidation, systems consolidation occurs within a time frame of days to years. For declarative memory, the latter is presumed to rely on an interaction between different brain regions, in particular the hippocampus and the medial prefrontal cortex (mPFC). Specifically, sleep has been proposed to provide a setting that supports such systems consolidation processes, leading to a transfer and perhaps transformation of memories. Using functional MRI, we show that postlearning sleep enhances hippocampal responses during recall of word pairs 48 h after learning, indicating intrahippocampal memory processing during sleep. At the same time, sleep induces a memory-related functional connectivity between the hippocampus and the mPFC. Six months after learning, memories activated the mPFC more strongly when they were encoded before sleep, showing that sleep leads to longlasting changes in the representation of memories on a systems level.fMRI ͉ hippocampus ͉ medial prefrontal cortex ͉ memory N ew memories must undergo a period of consolidation to become stable and immune to interference (1). Consolidation occurs in the form of molecular processes at individual synapses (2) but also in the form of systems consolidation, which is a reorganization of the memory trace within different brain systems (3)(4)(5). This is most obvious for declarative memory, where recall initially depends on the hippocampus, but after some time becomes hippocampus-independent (6-8). Instead, neocortical areas, especially the medial prefrontal cortex (mPFC), are assumed to take over its function (9,10). In a recent functional imaging study, Takashima et al. (11) showed that both regions display opposite activity over the course of 3 months; whereas the hippocampal contribution to memory recall decreases with time, the prefrontal one rises.During the last few years, an important contribution of sleep to memory consolidation has been revealed (12, 13). Sleep prevents forgetting and makes memories resistant to interference, especially when it closely follows learning (14, 15). In particular, animal research has shown that sleep provides the conditions for a hippocampal-neocortical dialogue and information transfer (16,17). Low levels of cholinergic neuromodulation disinhibit hippocampal-neocortical feedback synapses (18), and hippocampus and neocortex show synchronous activity during sleep (19). Together, these findings support the idea that sleep modifies the trace of a recently stored memory. In the present experiment, we tested this hypothesis using functional MRI (fMRI) to characterize brain activity related to free recall immediately, 48 h, and 6 months after learning a declarative memory task. The contribution of sleep to systems memory consolidation was tested by allowing subjects to sleep or by sleep depriving them during the first ...
BackgroundRelatively long duration retinal light exposure elicits nonvisual responses in humans, including modulation of alertness and cognition. These responses are thought to be mediated in part by melanopsin-expressing retinal ganglion cells which are more sensitive to blue light than violet or green light. The contribution of the melanopsin system and the brain mechanisms involved in the establishment of such responses to light remain to be established.Methodology/Principal FindingsWe exposed 15 participants to short duration (50 s) monochromatic violet (430 nm), blue (473 nm), and green (527 nm) light exposures of equal photon flux (1013ph/cm2/s) while they were performing a working memory task in fMRI. At light onset, blue light, as compared to green light, increased activity in the left hippocampus, left thalamus, and right amygdala. During the task, blue light, as compared to violet light, increased activity in the left middle frontal gyrus, left thalamus and a bilateral area of the brainstem consistent with activation of the locus coeruleus.Conclusion/SignificanceThese results support a prominent contribution of melanopsin-expressing retinal ganglion cells to brain responses to light within the very first seconds of an exposure. The results also demonstrate the implication of the brainstem in mediating these responses in humans and speak for a broad involvement of light in the regulation of brain function.
In humans, light enhances both alertness and performance during nighttime and daytime [1-4] and influences regional brain function [5]. These effects do not correspond to classical visual responses but involve a non-image forming (NIF) system, which elicits greater endocrine, physiological, neurophysiological, and behavioral responses to shorter light wavelengths than to wavelengths geared toward the visual system [6-11]. During daytime, the neural changes induced by light exposure, and their time courses, are largely unknown. With functional magnetic resonance imaging (fMRI), we characterized the neural correlates of the alerting effect of daytime light by assessing the responses to an auditory oddball task [12-15], before and after a short exposure to a bright white light. Light-induced improvement in subjective alertness was linearly related to responses in the posterior thalamus. In addition, light enhanced responses in a set of cortical areas supporting attentional oddball effects, and it prevented decreases of activity otherwise observed during continuous darkness. Responses to light were remarkably dynamic. They declined within minutes after the end of the light stimulus, following various region-specific time courses. These findings suggest that light can modulate activity of subcortical structures involved in alertness, thereby dynamically promoting cortical activity in networks involved in ongoing nonvisual cognitive processes.
In addition to classical visual effects, light elicits nonvisual brain responses, which profoundly influence physiology and behavior. These effects are mediated in part by melanopsin-expressing light-sensitive ganglion cells that, in contrast to the classical photopic system that is maximally sensitive to green light (550 nm), is very sensitive to blue light (470-480 nm). At present, there is no evidence that blue light exposure is effective in modulating nonvisual brain activity related to complex cognitive tasks. Using functional magnetic resonance imaging, we show that, while participants perform an auditory working memory task, a short (18 min) daytime exposure to blue (470 nm) or green (550 nm) monochromatic light (3 x 10(13) photons/cm2/s) differentially modulates regional brain responses. Blue light typically enhanced brain responses or at least prevented the decline otherwise observed following green light exposure in frontal and parietal cortices implicated in working memory, and in the thalamus involved in the modulation of cognition by arousal. Our results imply that monochromatic light can affect cognitive functions almost instantaneously and suggest that these effects are mediated by a melanopsin-based photoreceptor system.
Emotional events are usually better remembered than neutral ones. This effect is mediated in part by a modulation of the hippocampus by the amygdala. Sleep plays a role in the consolidation of declarative memory. We examined the impact of sleep and lack of sleep on the consolidation of emotional (negative and positive) memories at the macroscopic systems level. Using functional MRI (fMRI), we compared the neural correlates of successful recollection by humans of emotional and neutral stimuli, 72 h after encoding, with or without total sleep deprivation during the first post-encoding night. In contrast to recollection of neutral and positive stimuli, which was deteriorated by sleep deprivation, similar recollection levels were achieved for negative stimuli in both groups. Successful recollection of emotional stimuli elicited larger responses in the hippocampus and various cortical areas, including the medial prefrontal cortex, in the sleep group than in the sleep deprived group. This effect was consistent across subjects for negative items but depended linearly on individual memory performance for positive items. In addition, the hippocampus and medial prefrontal cortex were functionally more connected during recollection of either negative or positive than neutral items, and more so in sleeping than in sleep-deprived subjects. In the sleep-deprived group, recollection of negative items elicited larger responses in the amygdala and an occipital area than in the sleep group. In contrast, no such difference in brain responses between groups was associated with recollection of positive stimuli. The results suggest that the emotional significance of memories influences their sleep-dependent systems-level consolidation. The recruitment of hippocampo-neocortical networks during recollection is enhanced after sleep and is hindered by sleep deprivation. After sleep deprivation, recollection of negative, potentially dangerous, memories recruits an alternate amygdalo-cortical network, which would keep track of emotional information despite sleep deprivation.
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