Brain noise? Insomnia? Try A.S.M.R.

Fairyington does an interesting piece on a phenomenon called autonomous sensory meridian response (A.S.M.R.), which is felt as a mild calming tingling sensation that travels over the scalp or other part of the body in response to some kinds of subtle repetitive visual, auditory, or smell stimulation (rustling pages, whispering; tapping, scratching, etc.). The article contains numerous links to YouTube sites devoted to this effect. Some clips:

Carl W. Bazil, a sleep disorders specialist at Columbia University, says A.S.M.R. videos may provide novel ways to switch off our brains...“People who have insomnia are in a hyper state of arousal,” he said. “Behavioral treatments — guided imagery, progressive relaxation, hypnosis and meditation — are meant to try to trick your unconscious into doing what you want it to do. A.S.M.R. videos seem to be a variation on finding ways to shut your brain down.”

Bryson Lochte, a post-baccalaureate fellow at the National Institute on Drug Abuse who looked into A.S.M.R. for his senior thesis as a neuroscience major at Dartmouth College last year, has submitted his paper for publication in a scientific journal. Mr. Lochte said, “We focused on those areas in the brain associated with motivation, emotion and arousal to probe the effect A.S.M.R. has on the ‘reward system’ — the neural structures that trigger a dopamine surge amid pleasing reinforcements, like food or sex.

He compared A.S.M.R. to another idiosyncratic but well-studied sensation called musical frisson, which provokes a thrilling ripple of chills or goose bumps (technically termed piloerection) over one’s body in emotional response to music. Mathias Benedek, a research assistant at the University of Graz in Austria who co-authored two studies on emotion-provoked piloerection, says A.S.M.R. may be a softer, quieter version of the same phenomenon. “Frisson may simply be a stronger, full-blown response,” he said. And like A.S.M.R., the melodies that ignite frisson in one person may not in another.

Robert J. Zatorre, a professor of neuroscience at the Montreal Neurological Institute and Hospital at McGill University who has also studied musical frisson, said that “the upshot of my paper is that pleasurable music elicits dopamine activity in the striatum, which is a key component of the reward system” in the brain. Writing in The New York Times last year, in an article titled “Why Music Makes Our Brain Sing,” he notes, “What may be most interesting here is when this neurotransmitter is released: not only when the music rises to a peak emotional moment, but also several seconds before, during what we might call the anticipation phase.”

Perhaps the everyday experiences that A.S.M.R. videos capture — whispering, crinkling, opening and closing of boxes — evoke similar anticipatory mechanisms, sparking memories of past pleasures that we anticipate and relive each time we watch and listen.

Does phase of the moon influence our sleep? Three contradictory studies.

This is an update on a previous MindBlog posting. Vyazovskiy and Foster review three recent studies that give contradictory results on how or whether the phase of the moon influences our sleep. They note that the three studies compared data obtained from different subjects at different lunar phases and were biased and imbalanced in terms of age, gender, and many other factors. They suggest that in future research it should be mandatory to design within-subject experiments, rather than perform further retrospective studies. Here is their statement of the situation:

Whether the moon affects our sleep has intrigued our species since ancient times, but in the last decades only relatively few attempts have been made to address this issue with scientific rigor, and solid conclusions have been elusive [1]. A new cycle of research on the lunar effects on sleep was triggered by a retrospective study which carefully re-analyzed the sleep data collected under laboratory conditions in 33 subjects (age range 20–74 years) and showed clear cut effects of the lunar phase on several subjective and objective sleep parameters [2]. Specifically, EEG slow-wave activity (SWA), total sleep time and subjective sleep quality were reduced around the time of the full moon, while sleep latency and latency to REM sleep were prolonged. This study corroborated an earlier report [5], which found a significant decrease in the amount of subjective sleep around the full moon in 31 subjects (mean age of 50 years). This report triggered two further studies, published in the current issue, which either contradict or report novel effects of lunar phase 3 and 4.

One of these studies, a re-analysis of existing large data sets, could not confirm any of the findings made by Cajochen et al. [3]. By contrast, a second retrospective study [4], in which 47 young volunteers were analyzed, confirmed a decreased total sleep time around the full moon, but REM sleep latency was longer around the new moon. This contradicts the Cajochen et al. study as they found that the latency to REM was longest around the full moon [2].

References: 1. R.G. Foster, T. Roenneberg. Human responses to the geophysical daily, annual and lunar cycles. Curr. Biol., 18 (2008), pp. R784–R794 2. C. Cajochen, S. Altanay-Ekici, M. Munch, S. Frey, V. Knoblauch, A. Wirz-Justice. Evidence that the lunar cycle influences human sleep. Curr. Biol., 23 (2013), pp. 1485–1488 3. M. Cordi, S. Ackermann, F.W. Bes, F. Hartmann, B.N. Konrad, L. Genzel, M. Pawlowski, A. Steiger, H. Schulz, B. Rasch, M. Dresler. Lunar cycle effects on sleep and the file drawer problem. Curr. Biol., 24 (2014), pp. R549–R550 4. M. Smith, I. Croy, K.P. Waye. Human sleep and cortical reactivity are influenced by lunar phase. Curr. Biol., 24 (2014), pp. R551–R552 5. M. Roosli, P. Juni, C. Braun-Fahrlander, M.W. Brinkhof, N. Low, M. Egger. Sleepless night, the moon is bright: longitudinal study of lunar phase and sleep J. Sleep Res., 15 (2006), pp. 149–153

Sleep cleans our brains, renews our synapses, consolidates our memories

This bit of work got a flurry of attention recently, but I think is important enough to warrant repeating here.  Xie et al.  have used an elegant two-photon imaging technique to compare awake and sleeping mouse brains. They find that metabolic waste products of neural activity are cleared out of the sleeping brain at a faster rate than during the awake state:

...convective fluxes of interstitial fluid increased the rate of β-amyloid clearance during sleep. Thus, the restorative function of sleep may be a consequence of the enhanced removal of potentially neurotoxic waste products that accumulate in the awake central nervous system.

The review of this work by Underwood has a nice graphic of the fluid-filled channels (pale blue) that expand to flush out waste:

The role of sleep in memory consolidation is well known, and further work of Tononi's group has suggested that in rats, sleep maintains an overall synaptic balance, by uniformly dialing down synapses that have expanded their activity during the day. (I have also previously pointed to work on fruit flies by Tononi's group coming to a similar conclusion.)

Work of this sort suggests that the 50-70 million Americans who have insufficient sleep or some kind of sleep disorder (like sleep apnea) are carrying around extra garbage in their brains during the day and have brain synaptic connection that haven't recovered from previous days' activities, both factors that would seem likely to compromise our mental function!

Nighttime light impairs our emotional responses.

I have done a number of posts (enter melanopsin in the search box to find them) on a second visual system, involving the visual pigment melanopsin in our retinal ganglion cells, that has been shown to influence mood,memory, and cognition. Bedrosian et al. now add more detail to this story, showing that noctural light exposure, particularly to blue light, impairs emotional responses:

Life on earth is entrained to a 24 h solar cycle that synchronizes circadian rhythms in physiology and behavior; light is the most potent entraining cue. In mammals, light is detected by (1) rods and cones, which mediate visual function, and (2) intrinsically photosensitive retinal ganglion cells (ipRGCs), which primarily project to the suprachiasmatic nucleus (SCN) in the hypothalamus to regulate circadian rhythms. Recent evidence, however, demonstrates that ipRGCs also project to limbic brain regions, suggesting that, through this pathway, light may have a role in cognition and mood. Therefore, it follows that unnatural exposure to light may have negative consequences for mood or behavior. Modern environmental lighting conditions have led to excessive exposure to light at night (LAN), and particularly to blue wavelength lights. We hypothesized that nocturnal light exposure (i.e., dim LAN) would induce depressive responses and alter neuronal structure in hamsters (Phodopus sungorus). If this effect is mediated by ipRGCs, which have reduced sensitivity to red wavelength light, then we predicted that red LAN would have limited effects on brain and behavior compared with shorter wavelengths. Additionally, red LAN would not induce c-Fos activation in the SCN. Our results demonstrate that exposure to LAN influences behavior and neuronal plasticity and that this effect is likely mediated by ipRGCs. Modern sources of LAN that contain blue wavelengths may be particularly disruptive to the circadian system, potentially contributing to altered mood regulation.

A brain correlate of near death hallucinations and visions?

Borjigin et al. make some fascinating observations on brain activity that occurs during the moments of cardiac arrest when brain glucose levels have dropped precipitously. Activity associated with information processing briefly increases 8-fold, a burst even after 'clinical death.' Maybe this is why some patients can recall conversation happening in the operating room.

The brain is assumed to be hypoactive during cardiac arrest. However, the neurophysiological state of the brain immediately following cardiac arrest has not been systematically investigated. In this study, we performed continuous electroencephalography in rats undergoing experimental cardiac arrest and analyzed changes in power density, coherence, directed connectivity, and cross-frequency coupling. We identified a transient surge of synchronous gamma oscillations that occurred within the first 30 s after cardiac arrest and preceded isoelectric electroencephalogram. Gamma oscillations during cardiac arrest were global and highly coherent; moreover, this frequency band exhibited a striking increase in anterior–posterior-directed connectivity and tight phase-coupling to both theta and alpha waves. High-frequency neurophysiological activity in the near-death state exceeded levels found during the conscious waking state. These data demonstrate that the mammalian brain can, albeit paradoxically, generate neural correlates of heightened conscious processing at near-death.

Evidence that the Lunar cycle influences human sleep.

I have kept a log for many years that has convinced me that I have roughly monthly oscillations in motivation and libido, but I've not come across convincing evidence for roughly lunar or monthly cycles in men in literature searches. So, I perk up on seeing the examination by Cajochen et al. of sleep behavior under highly controlled conditions of a circadian laboratory study protocol without time cues. They find that subjective and objective measures of sleep vary according to lunar periodicity (~29.5 days). Subjects in the study were seventeen healthy young volunteers (nine women and eight men; age range, 20–31 years; mean, 25.0 ± 3.6 years [SD]) and 16 healthy older volunteers (eight women and eight men; age range, 57–74 years; mean, 65.0 ± 5.5 years) Here is their abstract:

Endogenous rhythms of circalunar periodicity (∼29.5 days) and their underlying molecular and genetic basis have been demonstrated in a number of marine species. In contrast, there is a great deal of folklore but no consistent association of moon cycles with human physiology and behavior. Here we show that subjective and objective measures of sleep vary according to lunar phase and thus may reflect circalunar rhythmicity in humans. To exclude confounders such as increased light at night or the potential bias in perception regarding a lunar influence on sleep, we retrospectively analyzed sleep structure, electroencephalographic activity during non-rapid-eye-movement (NREM) sleep, and secretion of the hormones melatonin and cortisol found under stringently controlled laboratory conditions in a cross-sectional setting. At no point during and after the study were volunteers or investigators aware of the a posteriori analysis relative to lunar phase. We found that around full moon, electroencephalogram (EEG) delta activity during NREM sleep, an indicator of deep sleep, decreased by 30%, time to fall asleep increased by 5 min, and EEG-assessed total sleep duration was reduced by 20 min. These changes were associated with a decrease in subjective sleep quality and diminished endogenous melatonin levels. This is the first reliable evidence that a lunar rhythm can modulate sleep structure in humans when measured under the highly controlled conditions of a circadian laboratory study protocol without time cues.

 

We can learn new information during sleep.

Arzi et al. have devised a nice demonstration of how we can learn new information during our sleep. They paired pleasant and unpleasant odors with different tones during sleep, and measured the subjects’ sniffs to tones alone when they were awake. Tones associated with pleasant smells produced stronger sniffs, and tones associated with disgusting smells produced weaker sniffs, despite the subjects’ lack of awareness of the learning process. The abstract:

During sleep, humans can strengthen previously acquired memories, but whether they can acquire entirely new information remains unknown. The nonverbal nature of the olfactory sniff response, in which pleasant odors drive stronger sniffs and unpleasant odors drive weaker sniffs, allowed us to test learning in humans during sleep. Using partial-reinforcement trace conditioning, we paired pleasant and unpleasant odors with different tones during sleep and then measured the sniff response to tones alone during the same nights' sleep and during ensuing wake. We found that sleeping subjects learned novel associations between tones and odors such that they then sniffed in response to tones alone. Moreover, these newly learned tone-induced sniffs differed according to the odor pleasantness that was previously associated with the tone during sleep. This acquired behavior persisted throughout the night and into ensuing wake, without later awareness of the learning process. Thus, humans learned new information during sleep.

Aging, sleep, and memory.

Events during a day that we think important to remember are held in short term memory storage by an active hippocampus. Then, during deep, non-REM, slow brain wave sleep, enhanced connectivity between the hippocampus and frontal cortex cortex allow transfer of the information to long term storage in frontal and temporal lobes. It is also know that the duration of this deep sleep diminishes as our frontal lobes diminish in size (atrophy) with aging. Mandor et al., in worked pointed to in an article by Benedict Carey, have done an interesting study suggesting that the interaction of these factors represents a neuropatholgical pathway associated with cognitive decline in later life. Here is their abstract:

Aging has independently been associated with regional brain atrophy, reduced slow wave activity (SWA) during non–rapid eye movement (NREM) sleep and impaired long-term retention of episodic memories. However, whether the interaction of these factors represents a neuropatholgical pathway associated with cognitive decline in later life remains unknown. We found that age-related medial prefrontal cortex (mPFC) gray-matter atrophy was associated with reduced NREM SWA in older adults, the extent to which statistically mediated the impairment of overnight sleep–dependent memory retention. Moreover, this memory impairment was further associated with persistent hippocampal activation and reduced task-related hippocampal-prefrontal cortex functional connectivity, potentially representing impoverished hippocampal-neocortical memory transformation. Together, these data support a model in which age-related mPFC atrophy diminishes SWA, the functional consequence of which is impaired long-term memory. Such findings suggest that sleep disruption in the elderly, mediated by structural brain changes, represents a contributing factor to age-related cognitive decline in later life.

Learning new information during sleep.

Arzi et al. do an ingenious experiment to show that we can do associative learning during our sleep. We can associate a sound with a pleasant or unpleasant odor and react, both while still asleep and after waking, with a deeper or shallower breath. This does not, however, represent the kind of 'sleep learning' long sought by students who unsuccessfully try to remember scientific or literary facts needed for an exam by playing a tape softly during sleep. Here is the abstract:

During sleep, humans can strengthen previously acquired memories, but whether they can acquire entirely new information remains unknown. The nonverbal nature of the olfactory sniff response, in which pleasant odors drive stronger sniffs and unpleasant odors drive weaker sniffs, allowed us to test learning in humans during sleep. Using partial-reinforcement trace conditioning, we paired pleasant and unpleasant odors with different tones during sleep and then measured the sniff response to tones alone during the same nights' sleep and during ensuing wake. We found that sleeping subjects learned novel associations between tones and odors such that they then sniffed in response to tones alone. Moreover, these newly learned tone-induced sniffs differed according to the odor pleasantness that was previously associated with the tone during sleep. This acquired behavior persisted throughout the night and into ensuing wake, without later awareness of the learning process. Thus, humans learned new information during sleep.

Rethinking sleep - brief wakeful resting boosts new memories over the long term.

Two recent articles point out that the prevailing notion that an eight hour chunk of sleep is required for optimum health and function is a relatively recent invention that doesn't take into account the usefulness of many varieties of sleep. Randall notes historical and contemporary evidence that other patterns are useful, and here is an abstract from Dewar et al. on how wakeful rest enhances long term consolidation of new memories:

A brief wakeful rest after new verbal learning enhances memory for several minutes. In the research reported here, we explored the possibility of extending this rest-induced memory enhancement over much longer periods. Participants were presented with two stories; one story was followed by a 10-min period of wakeful resting, and the other was followed by a 10-min period during which participants played a spot-the-difference game. In Experiment 1, wakeful resting led to significant enhancement of memory after a 15- to 30-min period and also after 7 days. In Experiment 2, this striking enhancement of memory 7 days after learning was demonstrated even when no retrievals were imposed in the interim. The degree to which people can remember prose after 7 days is significantly affected by the cognitive activity that they engage in shortly after new learning takes place. We propose that wakeful resting after new learning allows new memory traces to be consolidated better and hence to be retained for much longer.

Social jetlag and obesity.

Roenneberg et al. do an epidemiological study, showing that, beyond sleep duration, the difference between natural circadian sleep rhythm and the actual times of sleep people observe (social jetlag) is associated with increased body mass index. They suggest that living “against the clock” may be a factor contributing to the modern epidemic of obesity. (But... it seems to me people were doing this before the obesity epidemic was noted. Most experts attribute the epidemic to increased physical inactivity and abundance of cheap highly caloric foods.) Here is their summary and abstract:

-In 70% of the population, biological and social clocks differ by >1 hr (social jetlag) -Social jetlag is a predictor of BMI, especially for overweight individuals -The decrease of sleep duration over the past decade concerns only workdays -Individuals are progressively exposed to decreasing light, and their chronotypes delay

Abstract

Obesity has reached crisis proportions in industrialized societies. Many factors converge to yield increased body mass index (BMI). Among these is sleep duration. The circadian clock controls sleep timing through the process of entrainment. Chronotype describes individual differences in sleep timing, and it is determined by genetic background, age, sex, and environment (e.g., light exposure). Social jetlag quantifies the discrepancy that often arises between circadian and social clocks, which results in chronic sleep loss. The circadian clock also regulates energy homeostasis, and its disruption—as with social jetlag—may contribute to weight-related pathologies. Here, we report the results from a large-scale epidemiological study, showing that, beyond sleep duration, social jetlag is associated with increased BMI. Our results demonstrate that living “against the clock” may be a factor contributing to the epidemic of obesity. This is of key importance in pending discussions on the implementation of Daylight Saving Time and on work or school times, which all contribute to the amount of social jetlag accrued by an individual. Our data suggest that improving the correspondence between biological and social clocks will contribute to the management of obesity.

Don't go to bed angry...

Several studies have shown that sleep enhances emotional memories. Baran et al. show that maybe its better let anger keep you awake at night than to sleep on it. Sleep consolidates the negative emotional memory. Having trouble sleeping after an unsettling experience may be the brain's way of trying to keep the memory or emotion from being stored. The abstract:

Sleep enhances memories, particularly emotional memories. As such, it has been suggested that sleep deprivation may reduce posttraumatic stress disorder. This presumes that emotional memory consolidation is paralleled by a reduction in emotional reactivity, an association that has not yet been examined. In the present experiment, we used an incidental memory task in humans and obtained valence and arousal ratings during two sessions separated either by 12 h of daytime wake or 12 h including overnight sleep. Recognition accuracy was greater following sleep relative to wake for both negative and neutral pictures. While emotional reactivity to negative pictures was greatly reduced over wake, the negative emotional response was relatively preserved over sleep. Moreover, protection of emotional reactivity was associated with greater time in REM sleep. Recognition accuracy, however, was not associated with REM. Thus, we provide the first evidence that sleep enhances emotional memory while preserving emotional reactivity.

REM sleep chills out amygdala, reduces emotional reactivity

van der Helm et al. at Univ. of Cal. Berkeley have done interesting experiments in which 34 adults were randomly assigned to two groups which both performed an emotion reactivity test twice inside a functional magnetic resonance imaging (fMRI) scanner; separated by a 12 hr interval. The tests involved the rating and subsequent rerating of the same standard set of 150 affective picture stimuli. One group slept during the twelve hours interval with REM (rapid eye movement) sleep monitored by EEG, the other group was a control group that stayed awake during the day. Controls were done to eliminate possible time-of-day differences in emotional reactivity, independent of wake or sleep. Here is their abstract:

Clinical evidence suggests a potentially causal interaction between sleep and affective brain function; nearly all mood disorders display co-occurring sleep abnormalities, commonly involving rapid-eye movement (REM) sleep. Building on this clinical evidence, recent neurobiological frameworks have hypothesized a benefit of REM sleep in palliatively decreasing next-day brain reactivity to recent waking emotional experiences. Specifically, the marked suppression of central adrenergic neurotransmitters during REM (commonly implicated in arousal and stress), coupled with activation in amygdala-hippocampal networks that encode salient events, is proposed to (re)process and depotentiate previous affective experiences, decreasing their emotional intensity. In contrast, the failure of such adrenergic reduction during REM sleep has been described in anxiety disorders, indexed by persistent high-frequency electroencephalographic (EEG) activity (greater than 30 Hz); a candidate factor contributing to hyperarousal and exaggerated amygdala reactivity. Despite these neurobiological frameworks, and their predictions, the proposed benefit of REM sleep physiology in depotentiating neural and behavioral responsivity to prior emotional events remains unknown. Here, we demonstrate that REM sleep physiology is associated with an overnight dissipation of amygdala activity in response to previous emotional experiences, altering functional connectivity and reducing next-day subjective emotionality.

A nap enhances relational memory

Lau et al. make the following interesting observations:

It is increasingly evident that sleep strengthens memory. However, it is not clear whether sleep promotes relational memory, resultant of the integration of disparate memory traces into memory networks linked by commonalities. The present study investigates the effect of a daytime nap, immediately after learning or after a delay, on a relational memory task that requires abstraction of general concept from separately learned items. Specifically, participants learned English meanings of Chinese characters with overlapping semantic components called radicals. They were later tested on new characters sharing the same radicals and on explicitly stating the general concepts represented by the radicals. Regardless of whether the nap occurred immediately after learning or after a delay, the nap participants performed better on both tasks. The results suggest that sleep – even as brief as a nap – facilitates the reorganization of discrete memory traces into flexible relational memory networks.

Effects of blue light on our memory, cognition, and circadian thythm

I ran a vision research laboratory for 30 years,  and in the early 1970s found that installing natural spectrum florescent lights (with more blue wavelengths) in my research laboratory enhanced my relaxation and alertness. My graduate students and post-docs reported the same effect.  Following this subject I've done posts on work documenting this effect, and then subsequently finding that blue light is the best stimulus for a visual pathway that lies outside of the classical (red/green/blue) rod and cone photoreceptor cells of our retinas, driven by a the blue sensitive visual pigment melanopsin in some inner (ganglion) cells of the retina. The amygdala, at the core of our emotional brain, receives direct projections from these light sensitive retinal ganglion cells. Activation of this system also causes changes in brain areas related to working memory. An article by Beil now points to recent work noting consequences of the fact that that blue light is especially effective in suppressing the sleep promoting hormone melatonin that regulates our diurnal sleep-wake cycle. To examine the effects of energy-efficient light bulbs and electronic gadgets with LED screens that have greatly increased levels of blue light wavelengths, some researchers at the University of Basel:

...asked 13 men to sit before a computer each evening for two weeks before going to bed. During one week, for five hours every night, the volunteers sat before an old-style fluorescent monitor emitting light composed of several colors from the visible spectrum, though very little blue. Another week, the men sat at screens backlighted by light-emitting diodes, or LEDs. This screen was twice as blue...Melatonin levels in volunteers watching the LED screens took longer to rise at night, compared with when the participants were watching the fluorescent screens, and the deficit persisted throughout the evening...The subjects also scored higher on tests of memory and cognition after exposure to blue light...The finding adds to a series of others suggesting... that exposure to blue light may keep us more awake and alert, partly by suppressing production of melatonin. An LED screen bright enough and big enough could be giving an alert stimulus at a time that will frustrate the body’s ability to go to sleep later.

No sleep, better mood...

It is known that sleep deprivation leads to exaggerated neural and behavioral reactivity to negative, aversive experiences, but some patients with depression seem to perk up with lack of sleep. Gujar et al. now find that sleep deprivation also increases the reactivity of our brain reward networks, biasing us towards more positive appraisals of good emotional experiences. They did MRI measurements on 14 people who hadn't slept for about 36 hours while presenting them with emotionally neutral and pleasant-looking images. The volunteers rated a greater proportion of the images as 'pleasant' than did people who had maintained a normal sleep routine.:

....Using functional magnetic resonance imaging (fMRI), .. we demonstrate that sleep deprivation amplifies reactivity throughout human mesolimbic reward brain networks in response to pleasure-evoking stimuli. In addition, this amplified reactivity was associated with enhanced connectivity in early primary visual processing pathways and extended limbic regions, yet with a reduction in coupling with medial frontal and orbitofrontal regions. These neural changes were accompanied by a biased increase in the number of emotional stimuli judged as pleasant in the sleep-deprived group, the extent of which exclusively correlated with activity in mesolimbic regions. Together, these data support a view that sleep deprivation not only is associated with enhanced reactivity toward negative stimuli, but imposes a bidirectional nature of affective imbalance, associated with amplified reward-relevant reactivity toward pleasure-evoking stimuli also. Such findings may offer a neural foundation on which to consider interactions between sleep loss and emotional reactivity in a variety of clinical mood disorders.

Why old folks don’t sleep as well.

Older people have an earlier phase of everyday activity compared with the young. Not only is the consolidation of sleep and wake dramatically reduced, but overall circadian amplitude of hormones and body temperature are lower. Now Pagani et al. find that the biological clocks in cells taken from young and old people have the same periods, but they can be shortened by a heat labile factor in blood serum from older people. Identification of this factor might lead to development of drugs that block its action.:

Human aging is accompanied by dramatic changes in daily sleep–wake behavior: Activity shifts to an earlier phase, and the consolidation of sleep and wake is disturbed. Although this daily circadian rhythm is brain-controlled, its mechanism is encoded by cell-autonomous circadian clocks functioning in nearly every cell of the body. In fact, human clock properties measured in peripheral cells such as fibroblasts closely mimic those measured physiologically and behaviorally in the same subjects. To understand better the molecular mechanisms by which human aging affects circadian clocks, we characterized the clock properties of fibroblasts cultivated from dermal biopsies of young and older subjects. Fibroblast period length, amplitude, and phase were identical in the two groups even though behavior was not, thereby suggesting that basic clock properties of peripheral cells do not change during aging. Interestingly, measurement of the same cells in the presence of human serum from older donors shortened period length and advanced the phase of cellular circadian rhythms compared with treatment with serum from young subjects, indicating that a circulating factor might alter human chronotype. Further experiments demonstrated that this effect is caused by a thermolabile factor present in serum of older individuals. Thus, even though the molecular machinery of peripheral circadian clocks does not change with age, some age-related circadian dysfunction observed in vivo might be of hormonal origin and therefore might be pharmacologically remediable.

Competitions for memory, it's stabilization, and a memory enhancer

Kuhl et al. find that the competition in the brain between old memories and new ones that are associated with the same thing (for example, an old versus a new password, or yesterday's versus today's space in the parking lot) can be observed in fMRI. They found competition between visual memories was captured in the relative degree to which target vs. competing memories were reactivated within the ventral occipitotemporal cortex. When lowered VOTC reactivation indicated that conflict between target and competing memories was high, frontoparietal mechanisms were markedly engaged, revealing specific neural mechanisms that tracked competing mnemonic evidence.

In another study on memory Diekelmann et al. show that memory reactivation has opposing effects on memory stability during wakefulness and sleep. Reactivation during slow-wave sleep following learning can stabilize memories. Reactivation during wakefulness has the opposite effect, rendering memories labile and susceptible to modest modification.

Finally Benedict Carey points to a study by Shema et al. showing that increasing levels of a brain enzyme (a protein kinase C isoform) involved in memory formation enhances long term memory. Also, Chen et al. show that injections of a different protein, a growth factor involved in memory formation (insulin-like growth factor II) can have the same effect.

Sleep deprivation biases economic risk-taking.

Venkatraman et al. make these fascinating observations:

A single night of sleep deprivation (SD) evoked a strategy shift during risky decision making such that healthy human volunteers moved from defending against losses to seeking increased gains. This change in economic preferences was correlated with the magnitude of an SD-driven increase in ventromedial prefrontal activation as well as by an SD-driven decrease in anterior insula activation during decision making. Analogous changes were observed during receipt of reward outcomes: elevated activation to gains in ventromedial prefrontal cortex and ventral striatum, but attenuated anterior insula activation following losses. Finally, the observed shift in economic preferences was not correlated with change in psychomotor vigilance. These results suggest that a night of total sleep deprivation affects the neural mechanisms underlying economic preferences independent of its effects on vigilant attention.

Sleep enhances memories relevant to the future.

Here is a fascinating bit of work from Wilhelm et al., which possibly explains why in my first moments of starting to awaken, I notice that finger sequences of piano pieces I am studying to perform are playing in my head....

The brain encodes huge amounts of information, but only a small fraction is stored for a longer time. There is now compelling evidence that the long-term storage of memories preferentially occurs during sleep. However, the factors mediating the selectivity of sleep-associated memory consolidation are poorly understood. Here, we show that the mere expectancy that a memory will be used in a future test determines whether or not sleep significantly benefits consolidation of this memory. Human subjects learned declarative memories (word paired associates) before retention periods of sleep or wakefulness. Postlearning sleep compared with wakefulness produced a strong improvement at delayed retrieval only if the subjects had been informed about the retrieval test after the learning period. If they had not been informed, retrieval after retention sleep did not differ from that after the wake retention interval. Retention during the wake intervals was not affected by retrieval expectancy. Retrieval expectancy also enhanced sleep-associated consolidation of visuospatial (two-dimensional object location task) and procedural motor memories (finger sequence tapping). Subjects expecting the retrieval displayed a robust increase in slow oscillation activity and sleep spindle count during postlearning slow-wave sleep (SWS). Sleep-associated consolidation of declarative memory was strongly correlated to slow oscillation activity and spindle count, but only if the subjects expected the retrieval test. In conclusion, our work shows that sleep preferentially benefits consolidation of memories that are relevant for future behavior, presumably through a SWS-dependent reprocessing of these memories.