CiteULike: pussywillow's library [56 articles]

Functional MRI during sleep: BOLD signal decreases and their electrophysiological correlates.

M Czisch — 2005-02-18T22:03:45-00:00

Eur J Neurosci, Vol. 20, No. 2. (July 2004), pp. 566-574.

Prominent local decreases in blood oxygenation level (BOLD) can be observed by functional magnetic resonance imaging (fMRI) upon acoustic stimulation during sleep. The goal of this study was to further characterize this BOLD signal decrease with respect to corresponding neurophysiological phenomena using a simultaneous electroencephalography (EEG)/fMRI approach in sleeping human subjects. Healthy volunteers were subjected to acoustic stimulation during non-rapid eye movement (NREM) sleep. On the basis of statistical parametric maps, the correlations between the fMRI response (both amplitude and extent of the BOLD response) and the concomittant changes in the EEG (delta power and K-complexes) were calculated. Amplitude and extent of the stimulus-induced negative BOLD effect correlated positively with measures of EEG synchronization, namely an increase in the number of K-complexes and EEG delta power. Stimulus-induced BOLD decreases were most prominent during light (stage 2) NREM sleep and disappeared during slow wave sleep, indicating an influence of the baseline degree of hyperpolarization. Our observations provide first evidence that 'negative' BOLD signal changes during human sleep are associated with electrophysiological indicators of altered neuronal activity. Increased number of K-complexes and delta power reflecting hyperpolarization suggests true cortical deactivation upon stimulus presentation. This sleep stage-dependent deactivation might serve to protect the brain from arousing stimuli, particularly during the light phases of sleep shortly after sleep onset.

IL-6 and its circadian secretion in humans

AN Vgontzas — 2008-04-14T09:16:24-00:00

Neuroimmunomodulation, Vol. 12, No. 3. (2005), pp. 131-40.

Interleukin-6 (IL-6) is a pleiotropic cytokine produced by numerous types of immune and nonimmune cells and is involved in many pathophysiologic mechanisms in humans. Many studies suggest that IL-6 is a putative 'sleep factor' and its circadian secretion correlates with sleep/sleepiness. IL-6 is elevated in disorders of excessive daytime sleepiness such as narcolepsy and obstructive sleep apnea. It correlates positively with body mass index and may be a mediator of sleepiness in obesity. Also the secretion of this cytokine is stimulated by total acute or partial short-term sleep loss reflecting the increased sleepiness experienced by sleep-deprived individuals. Studies that evaluated the 24-hour secretory pattern of IL-6 in healthy young adults suggest that IL-6 is secreted in a biphasic circadian pattern with two nadirs at about 08.00 and 21.00, and two zeniths at about 19.00 and 05.00 h. In contrast, following sleep deprivation or in disorders of sleep disturbance, e.g., insomnia, IL-6 peaks during the day and, based on the level of stress system activity, i.e., cortisol secretion, contributes to either sleepiness and deep sleep (low cortisol) or feelings of tiredness and fatigue and poor sleep (high cortisol). In order to address concerns about the potential impact of differences of IL-6 levels between the beginning and the end of the 24-hour blood-drawing experiment, we proceeded with a cosinor analysis of 'detrended' data in young and old healthy individuals. This new analysis did not affect the biphasic circadian pattern of IL-6 secretion in young adults, while it augmented the flattened circadian pattern in old individuals in whom the difference was greater. Finally, IL-6 appears to be somnogenic in rats and exhibits a diurnal rhythm that follows the sleep/wake cycle in these animals. We conclude that IL-6 is a mediator of sleepiness and its circadian pattern reflects the homeostatic drive for sleep.

Subjective fatigue and subjective sleepiness: two independent consequences of sleep disorders?

Jamil Hossain — 2005-08-31T09:36:25-00:00

Journal of Sleep Research, Vol. 14, No. 3. (September 2005), pp. 245-253.

Cerebral blood flow and oxygen metabolism during mild hypothermia in patients with subarachnoid haemorrhage.

S Kawamura — 2006-12-14T07:03:34-00:00

Acta Neurochir (Wien), Vol. 142, No. 10. (2000)

Cerebral blood flow and O2 metabolism during hypothermia (33-34 degrees C) was evaluated in 5 patients with aneurysmal subarachnoid haemorrhage by positron emission tomography (PET). Their preoperative clinical condition was WFNS scale IV or V. The patients received surface cooling postoperatively, and were maintained in a hypothermic state during transfer for radiological examination. Positron emission tomography revealed a decrease in cerebral blood flow and O2 metabolic rate. Cerebral blood flow was 34.8+/-15.1 ml/100 ml/min and the O2 metabolic rate was 1.85+/-0.61 ml/100 ml/min in areas of the middle cerebral artery ipsilateral to the ruptured aneurysms, whereas these values were 30.8+/-7.1 and 2.21+/-0.45 ml/100 ml/min, respectively, on the contralateral side. This represents a decrease of 37+/-27% compared to normal cerebral blood flow and 52+/-16% compared to normal O2 metabolic rate (p < 0.02) in the ipsilateral areas, and decreases of 44+/-13% and 43+/-12%, respectively, on the contralateral side. The present results reflected the luxury perfusion state in almost all cases and provide the first PET evidence of decreased cerebral blood flow and metabolic rate of O2 during hypothermia in humans.

Time of day accounts for overnight improvement in sequence learning.

A Keisler — 2008-05-09T16:46:13-00:00

Learning & memory (Cold Spring Harbor, N.Y.), Vol. 14, No. 10. (2007), pp. 669-672.

The theory that certain skills improve with a night of sleep has received considerable interest in recent years. However, because sleep typically occurs at the same time of day in humans, it is difficult to separate the effects of sleep from those of time of day. By using a version of the Serial Response Time Task, we assessed the role of sleep in implicit sequence learning while controlling for possible time-of-day effects. We replicated the apparent benefit of sleep on human participants. However, our data show that sleep does not affect implicit sequence learning; rather, time of day affects the ability of participants to express what they have learned.

Why we sleep: the temporal organization of recovery.

E Mignot — 2008-05-07T20:52:53-00:00

PLoS biology, Vol. 6, No. 4. (29 April 2008)

The sleep-modulating peptide cortistatin augments the h-current in hippocampal neurons.

P Schweitzer — 2005-07-28T09:30:05-00:00

J Neurosci, Vol. 23, No. 34. (26 November 2003), pp. 10884-10891.

Cortistatin (CST) is a sleep-modulating peptide found exclusively in the brain. Although CST is closely related to somatostatin (SST) and binds to SST receptors, CST has effects on sleep and neuronal activity in cortex and hippocampus that differ from SST. To uncover the cellular mechanisms affected by CST, we studied the electrophysiological postsynaptic effects of CST and assessed its interaction with SST on hippocampal CA1 pyramidal neurons. CST altered intrinsic membrane properties and occluded SST effects, indicating that both peptides similarly augment the sustained K+ M- and leak-currents (IM and IK(L)). In the presence of SST, however, CST elicited an additional inwardly rectifying component in the hyperpolarized range. This effect was unaffected by barium, used to block K+ currents, but was completely prevented by the selective h-current (Ih) blocker ZD7288. CST, but not SST, selectively increased Ih in a concentration-dependent manner by augmenting its maximum conductance. CST did not shift the Ih activation curve, and the peptide effect was unaffected by a membrane-permeable analog of cAMP. We conclude that CST and SST similarly increase K+ conductances in hippocampal neurons, most likely by activating SST receptors. However, CST additionally augments Ih, a voltage-dependent current that plays a key role in the modulation of synaptic integration and regulates oscillatory activity. Our results indicate that CST targets a specific conductance unaffected by SST to modulate cellular mechanisms implicated in sleep regulation.

Sleep and arousal: thalamocortical mechanisms.

DA McCormick — 2005-07-29T10:20:41-00:00

Annu Rev Neurosci, Vol. 20 (1997), pp. 185-215.

Thalamocortical activity exhibits two distinct states: (a) synchronized rhythmic activity in the form of delta, spindle, and other slow waves during EEG-synchronized sleep and (b) tonic activity during waking and rapid-eye-movement sleep. Spindle waves are generated largely through a cyclical interaction between thalamocortical and thalamic reticular neurons involving both the intrinsic membrane properties of these cells and their anatomical interconnections. Specific alterations in the interactions between these cells can result in the generation of paroxysmal events resembling absence seizures in children. The release of several different neurotransmitters from the brain stem, hypothalamus, basal forebrain, and cerebral cortex results in a depolarization of thalamocortical and thalamic reticular neurons and an enhanced excitability in many cortical pyramidal cells, thereby suppressing the generation of sleep rhythms and promoting a state that is conducive to sensory processing and cognition.

Parkinsonism with excessive daytime sleepiness A narcolepsy-like disorder?

C Baumann — 2005-03-07T22:45:11-00:00

J Neurol, Vol. 252, No. 2. (February 2005), pp. 139-145.

BACKGROUND : Parkinsonian patients with excessive daytime sleepiness (EDS), hallucinations, REM sleep behavior disorder (RBD), short mean sleep latencies, and sleep-onset REM periods (SOREMP) on multiple sleep latency tests (MSLT) have been reported. In these patients a narcolepsy-like pathophysiology of sleep-wake disturbances has been suggested. PATIENTS AND METHODS : We studied 14 consecutive patients with Parkinsonism and EDS. Standard studies included assessment of duration and severity of Parkinsonism (Hoehn & Yahr score), Epworth sleepiness score (ESS), history of "REM-symptoms" (RBD/hallucinations/sleep paralysis/cataplexy-like episodes), polysomnography (PSG),MSLT, and measurement of cerebrospinal fluid (CSF) levels of hypocretin-1 (orexin A). RESULTS : There were 12 men and 2 women (mean age 69 years; range 54-82). The mean duration and the Hoehn & Yahr score were 6.3 years and 2.2, respectively. Diagnoses included idiopathic Parkinson's disease (IPD, n=10), dementia with diffuse Lewy bodies (n=3), and multisystem atrophy (n=1). The ESS was >/=10 in all patients (mean 12; range 10-18). "REM-symptoms" were reported by all but two patients (hallucinations: n=9; RBD: n=9).None of the patients reported cataplexy-like symptoms or sleep paralysis. On PSG sleep apnea (apnea hypopnea index > 10/h, n=7), periodic limb movements during sleep (PLMS-index > 10/h, n=6), and features of RBD (n=5) were found. On MSLT mean sleep latency was < 5 minutes in 10 patients, and SOREMP were found in two patients. When compared with controls (n=20, mean 497 pg/ml; range 350-603), CSF hypocretin-1 levels were normal in 8 patients and low in 2 patients (221 and 307 pg/ml, respectively). CONCLUSION : These findings do not support the hypothesis of a "final common pathway" in the pathophysiology of narcolepsy and Parkinsonism with EDS. Sleep apnea and PLMS may play a so-far underestimated role in the pathogenesis of EDS in Parkinsonian patients.

Neurophysiological correlates of sleepiness: A combined TMS and EEG study

Luigi De Gennaro — 2007-07-05T03:58:55-00:00

NeuroImage, Vol. 36, No. 4. (15 July 2007), pp. 1277-1287.

Changes of cortical and corticospinal excitability as a function of sleep deprivation have been studied, using EEG power maps and several TMS measures in 33 normal subjects before and after a 40-h sleep deprivation (SD). The effects of SD were independently assessed by subjective and EEG measures of sleepiness, the latter being represented in terms of cortical maps for different frequency bands. Short intracortical facilitation (SICF) and inhibition (SICI) were measured by the paired-pulse TMS technique with different inter-stimulus intervals. Besides standardized motor threshold (MT), lower threshold (LT) and upper threshold (UT) were also determined. Subjective sleepiness severely increased as a consequence of SD, paralleled by a drastic decrease of alertness. EEG topography showed large increases in delta and theta activity, mainly evident at fronto-central areas. Standard MTs, as well as LTs and UTs, all increased as a consequence of SD. SICF also showed a significant increase as compared to pre-deprivation values, but only in females. The increase of theta activity was strongly associated in the left frontal and prefrontal cortex to a smaller decrease of corticospinal excitability, expressed by MTs, and a larger increase of intracortical facilitation, expressed by SICF. TMS and EEG measures converge in indicating that SD has severe effects on both cortical and corticospinal excitability, as shown respectively by the increases of slow-frequency EEG power and MTs. The SICF enhancement in females and the results of the combined topographical analysis of EEG and TMS changes are coherent with the hypothesis that cortical TMS-evoked responses are higher as a consequence of a longer wakefulness. However, the lack of an increase in cortical excitability after prolonged wakefulness in males suggests some caution in the generalization of these effects, that deserve further investigation.

Coalescence of sleep rhythms and their chronology in corticothalamic networks.

M Steriade — 2008-01-09T13:27:18-00:00

Sleep Res Online, Vol. 1, No. 1. (1998), pp. 1-10.

The cellular substrates of sleep oscillations have recently been investigated by means of multi-site, intracellular and extracellular recordings under anesthesia, and these data have been validated during natural sleep in cats and humans. Although various rhythms occurring during the state of resting sleep (spindle, 7-14 Hz; delta, 1-4 Hz; and slow oscillation, <1 Hz) are conventionally described by using their different frequencies, they are coalesced within complex wave-sequences due to the synchronizing power of the cortically generated slow oscillation (main peak around 0.7 Hz). In intracellular recordings from anesthetized animals, the slow oscillation is characterized by a biphasic sequence consisting of a prolonged hyperpolarization and depolarization. Basically similar patterns are observed by means of extracellular discharges and/or field potentials in naturally sleeping animals and humans. The depolarizing component of the slow oscillation is transferred to the thalamus where it contributes to the synchronization of spindles over widespread territories. The association between the depolarizing component of the slow oscillation and the subsequent sequence of spindle waves forms what is termed the K-complex. The slow oscillation also groups cortically generated delta waves. At variance with previous assumptions that the brain lies for the most part in the dark and a global inhibition occurs in resting sleep, cortical cells are quite active in this behavioral state. This unexpectedly rich activity raises the possibility that, during sleep, the brain is occupied to specify/reorganize circuits and to consolidate memory traces acquired during wakefulness.

Regional Cerebral Blood Flow Changes as a Function of Delta and Spindle Activity during Slow Wave Sleep in Humans

Nina Hofle — 2008-04-28T16:46:12-00:00

J. Neurosci., Vol. 17, No. 12. (15 June 1997), pp. 4800-4808.

Thermoregulation as a sleep signalling system.

SS Gilbert — 2005-11-12T23:17:21-00:00

Sleep Med Rev, Vol. 8, No. 2. (April 2004), pp. 81-93.

Temperature and sleep are interrelated processes. Under normal environmental conditions, the rhythms of core body temperature Tc and sleep propensity vary inversely across the day and night in healthy young adults. Although this relationship has drawn considerable interest, particularly in recent years, it is still not known whether this relationship is causative or merely coincidental. As somnogenic brain areas contain thermosensitive cells, it is possible that the sleep/wake cycle may be directly affected by thermoregulatory changes themselves. That is, that changes in temperature may trigger, either directly or indirectly, somnogenic brain areas to initiate sleep. There is now an emerging body of evidence from both physiological and neuroanatomical studies to indicate that this may indeed be the case. This paper will examine the literature relating to this relationship and propose a model where thermoregulatory changes provide an additional signal to the brain regions that regulate sleep and wakefulness. The model attempts to explain how temperature changes before and after sleep onset act in a positive feedback loop to maintain a consolidated sleep bout.

Sleep on it: cortical reorganization after-the-fact.

KL Hoffman — 2006-05-03T09:32:57-00:00

Trends Neurosci, Vol. 25, No. 1. (January 2002), pp. 1-2.

Sleep can facilitate memory formation, but its role in cortical plasticity is poorly understood. A recent study found that sleep, following monocular deprivation (MD), facilitated cortical changes in ocular dominance. The magnitude of plasticity was similar to that observed after continued MD, and larger than that seen after sleep deprivation in darkness, suggesting that sleep per se enables mechanisms of cortical plasticity. Experience-dependent plasticity during sleep could be part of a more global process of memory consolidation.

The Role of Sleep in Memory Consolidation and Brain Plasticity: Dream or Reality?

Marcos Frank — 2008-04-24T22:13:23-00:00

Neuroscientist, Vol. 12, No. 6. (1 December 2006), pp. 477-488.

The notion that a good night of sleep improves memory is widely accepted by the general public. Among sleep scientists, however, the idea has been hotly debated for decades. In this review, the authors consider current evidence for and against the hypothesis that sleep facilitates memory consolidation and promotes plastic changes in the brain. They find that despite a steady accumulation of positive findings over the past decade, the precise role of sleep in memory and brain plasticity remains elusive. This impasse may be resolved by more integrated approaches that combine behavioral and neurophysiological measurements in well-described in vivo models of synaptic plasticity. 10.1177/1073858406293552

Mechanisms of arousal from sleep and their consequences.

GS Gilmartin — 2006-04-08T09:29:26-00:00

Curr Opin Pulm Med, Vol. 10, No. 6. (November 2004), pp. 468-474.

PURPOSE OF REVIEW: In recent years, understanding of the mechanisms by which sleep is maintained and the consequences of abnormal arousal from sleep has improved rapidly. This review describes the recent insights into the nature of sleep and arousal and the particular insights gained in common disease states such as sleep-disordered breathing. RECENT FINDINGS: Expansion of the definitions of the classic stages of non-REM and REM sleep to include consideration of the role of cyclic alternating pattern sleep as a gating mechanism for arousal and maintenance of stable sleep has led to a significant advancement in understanding the nature of normal and pathologic arousals from sleep. In addition, the effect of arousals from sleep on cerebral cortical electrophysiology and autonomic activation has been further defined, with a potential effect on clinical practice. SUMMARY: Arousal from sleep is dependent on wake-promoting influences overwhelming forces promoting sleep. Autonomic activation and cortical arousal can significantly affect and destabilize sleep homeostasis. The understanding of sleep-respiration interactions continues to evolve. The definition of the minimal arousal event is an important research goal. It will be important in clinical practice and research to consider sleep stability domains as a complement to sleep depth staging to allow better understanding of the relative stability and instability of the system and to consider all components of the consequences of arousal.

Functional Imaging of Working Memory after 24 Hr of Total Sleep Deprivation

Michael Chee — 2008-01-19T08:55:54-00:00

J. Neurosci., Vol. 24, No. 19. (12 May 2004), pp. 4560-4567.

The neurobehavioral effects of 24 hr of total sleep deprivation (SD) on working memory in young healthy adults was studied using functional magnetic resonance imaging. Two tasks, one testing maintenance and the other manipulation and maintenance, were used. After SD, response times for both tasks were significantly slower. Performance was better preserved in the more complex task. Both tasks activated a bilateral, left hemisphere-dominant frontal-parietal network of brain regions reflecting the engagement of verbal working memory. In both states, manipulation elicited more extensive and bilateral (L>R) frontal, parietal, and thalamic activation. After SD, there was reduced blood oxygenation level-dependent signal response in the medial parietal region with both tasks. Reduced deactivation of the anterior medial frontal and posterior cingulate regions was observed with both tasks. Finally, there was disproportionately greater activation of the left dorsolateral prefrontal cortex and bilateral thalamus when manipulation was required. This pattern of changes in activation and deactivation bears similarity to that observed when healthy elderly adults perform similar tasks. Our data suggest that reduced activation and reduced deactivation could underlie cognitive impairment after SD and that increased prefrontal and thalamic activation may represent compensatory adaptations. The additional left frontal activation elicited after SD is postulated to be task dependent and contingent on task complexity. Our findings provide neural correlates to explain why task performance in relatively more complex tasks is better preserved relative to simpler ones after SD. 10.1523/JNEUROSCI.0007-04.2004

Lights Out: Sleep, Sugar, and Survival

TS Wiley — 2007-08-22T15:40:25-00:00

(27 February 2001)

<CENTER>When it comes to obesity, diabetes, heart disease, cancer, and depression, everything you believe is a lie.</CENTER>Lights OutWith research gleaned from the National Institutes of Health, T.S. Wiley and Bent Formby deliver staggering findings: Americans really are sick from being tired. Diabetes, heart disease, cancer, and depression are rising in our population. We're literally dying for a good night's sleep.Our lifestyle wasn't always this way. It began with the invention of the lightbulb.When we don't get enough sleep in sync with seasonal light exposure, we fundamentally alter a balance of nature that has been programmed into our physiology since Day One. This delicate biological rhythm rules the hormones and neurotransmitters that determine appetite, fertility, and mental and physical health. When we rely on artificial light to extend our day until 11 PM, midnight, and beyond, we fool our bodies into living in a perpetual state of summer. Anticipating the scarce food supply and forced inactivity of winter, our bodies begin storing fat and slowing metabolism to sustain us through the months of hibernation and hunger that never arrive.Our own survival instinct, honed over millennia, is now killing us.Wiley and Formby also reveal:<UL TYPE=DISC> <LI>That studies from our own government research prove the role of sleeplessness in diabetes, heart disease, cancer, infertility, mental illness, and premature aging; <LI>Why the carbohydrate-rich diets recommended by many health professionals are not only ridiculously ineffective but deadly; <LI>Why the lifesaving information that can turn things around is one of the best-kept secrets of our day.</UL>Lights Out is one wake-up call none of us can afford to miss. We all know we don't get enough sleep. What we don't know is that there is a killer connection between sleep, food, light, and health. And that when it comes to obesity, diabetes, heart disease, cancer, and depression, you need to rethink everything you know. Based on years of research at the National Institute of Health, Kept in the Dark will tell you: -- Why weight-loss is as easy as the flick of a switch -- Why researchers can give mice cancer just by leaving the lights on -- Why exercise can really give you a heart attack -- Why Type II diabetes has increased four-fold and why you're next -- Why you're overproducing sex hormones but you're too tired to want sex -- Why infertility plagues Baby Boomers -- Why we're a Prozac Nation and still fight depression constantly -- Why you'll go the way of the dinosaurs if you don't eat and sleep in sync with the spin of the planet

State transitions between wake and sleep, and within the ultradian cycle, with focus on the link to neuronal activity.

H Merica — 2006-04-08T09:26:25-00:00

Sleep Med Rev, Vol. 8, No. 6. (December 2004), pp. 473-485.

The structure of sleep across the night as expressed by the hypnogram, is characterised by repeated transitions between the different states of vigilance: wake, light and deep non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep. This review is concerned with current knowledge on these state transitions, focusing primarily on those findings that allow the integration of data at cellular level with spectral time-course data at the encephalographic (EEG) level. At the cellular level it has been proposed that, under the influence of circadian and homeostatic factors, transitions between wake and sleep may be determined by mutually inhibitory interaction between sleep-active neurons in the hypothalamic preoptic area and wake-active neurons in multiple arousal centres. These two fundamentally different behavioural states are separated by the sleep onset and the sleep inertia periods each characterised by gradual changes in which neither true wake nor true sleep patterns are present. The results of sequential spectral analysis of EEG data on moves towards and away from deep sleep are related to findings at the cellular level on the generating mechanisms giving rise to the various NREM oscillatory modes under the neuromodulatory control of brainstem-thalamic activating systems. And there is substantial evidence at cellular level that transition to and from REM sleep is governed by the reciprocal interaction between cholinergic REM-on neurons and aminergic REM-off neurons located in the brainstem. Similarity between the time-course of the REM-on neuronal activity and that of EEG power in the high beta range (approximately 18-30 Hz) allows a tentative parallelism to be drawn between the two. This review emphasises the importance of the thalamically projecting brainstem activating systems in the orchestration of the transitions that give rise to state progression across the sleep-wake cycle.

Sleep-dependent memory consolidation and reconsolidation.

R Stickgold — 2008-01-29T13:37:15-00:00

Sleep Med, Vol. 8, No. 4. (June 2007), pp. 331-343.

Molecular, cellular, and systems-level processes convert initial, labile memory representations into more permanent ones, available for continued reactivation and recall over extended periods of time. These processes of memory consolidation and reconsolidation are not all-or-none phenomena, but rather a continuing series of biological adjustments that enhance both the efficiency and utility of stored memories over time. In this chapter, we review the role of sleep in supporting these disparate but related processes.

Sleeping newborns extract prosody from continuous speech.

Anke Sambeth — 2007-12-20T11:30:42-00:00

Clin Neurophysiol (7 December 2007)

OBJECTIVE: Behavioral experiments show that infants use both prosodic and statistical cues in acquiring language. However, it is not yet clear whether these prosodic and statistical tools are already present at birth. METHODS: We recorded brain responses of sleeping newborns to natural sounds rich in prosody, namely singing and continuous speech, and to two impoverished manipulations of speech. A total of 11 newborns were presented with continuous speech, singing, and degraded speech, while MEG was recorded. RESULTS: We found that a brain response elicited to the prosodically rich singing and continuous natural speech conditions decreased dramatically when the prosody in the speech was impoverished. CONCLUSIONS: We claim that this response is the indicator of the infants' sensitivity to prosodic cues in language, which is already present at birth during natural sleep. SIGNIFICANCE: The indicators of detection of prosody may be crucial in assessing the normal and abnormal cortical function in newborns, especially of those infants at-risk for language problems.

Awaking and Sleeping a Complex Network

R Lopez-Ruiz — 2004-11-22T00:17:30-00:00

(23 June 2004)

A network with local dynamics of logistic type is considered. We implement a mean-field multiplicative coupling among first-neighbor nodes. When the coupling parameter is small the dynamics is dissipated and there is no activity: the network is turned off. For a critical value of the coupling a non-null stable synchronized state, which represents a turned on network, emerges. This global bifurcation is independent of the network topology. We characterize the bistability of the system by studying how to perform the transition, which now is topology dependent, from the active state to that with no activity, for the particular case of a scale free network. This could be a naive model for the wakening and sleeping of a brain-like system.

Sleeping sickness and the brain.

B Enanga — 2007-03-31T02:40:59-00:00

Cell Mol Life Sci, Vol. 59, No. 5. (May 2002), pp. 845-858.

Recent progress in understanding the neuropathological mechanisms of sleeping sickness reveals a complex relationship between the trypanosome parasite that causes this disease and the host nervous system. The pathology of late-stage sleeping sickness, in which the central nervous system is involved, is complicated and is associated with disturbances in the circadian rhythm of sleep. The blood-brain barrier, which separates circulating blood from the central nervous system, regulates the flow of materials to and from the brain. During the course of disease, the integrity of the blood-brain barrier is compromised. Dysfunction of the nervous system may be exacerbated by factors of trypanosomal origin or by host responses to parasites. Microscopic examination of cerebrospinal fluid remains the best way to confirm late-stage sleeping sickness, but this necessitates a risky lumbar puncture. Most drugs, including many trypanocides, do not cross the blood-brain barrier efficiently. Improved diagnostic and therapeutic approaches are thus urgently required. The latter might benefit from approaches which manipulate the blood-brain barrier to enhance permeability or to limit drug efflux. This review summarizes our current understanding of the neurological aspects of sleeping sickness, and envisages new research into blood-brain barrier models that are necessary to understand the interactions between trypanosomes and drugs active against them within the host nervous system.

The dreaming mind-brain: a Jungian perspective.

M Wilkinson — 2007-06-27T17:56:06-00:00

J Anal Psychol, Vol. 51, No. 1. (February 2006), pp. 43-59.

In this paper I discuss the nature and role of dream and the dreaming process in Jungian clinical practice in the light of neuroscience. Insights from contemporary neuroscience support rather than contest Jung's view that emotional truth, not censorship or disguise, underpins the dreaming process. I use clinical material to illustrate how work with dreams within the total interactive experience of the analytic dyad enables the development of the emotional scaffolding necessary for the development of 'mind'. Large scale evidence-based research reveals that dreaming is caused by brain activity during sleep that is both biochemically and regionally different from that of waking states. Recent imaging studies confirm that dreams are the mind's vehicle for the processing of emotional states of being, particularly the fear, anxiety, anger or elation that often figure prominently. Dream sleep is understood as also being the guardian of memory, playing a part in forgetting, encoding and affective organization of memory. In the clinical section of the paper I let a series of dreams speak for themselves, revealing the emotionally salient concerns of the dreamer, weaving past and present, transference and reality together in a way that demonstrates the healthy attempt of the brain-mind to come to terms with difficult emotional experience from the past. The dreams become dreamable as part of the meaning-making process of analysis.

Dreaming, Adaptation, and Consciousness.The Social Mapping Hypothesis

Derek Brereton — 2006-08-17T17:55:51-00:00

Ethos, Vol. 28, No. 3. (2000), pp. 379-409.

This article develops and tests the social mapping hypothesis, namely, that the neurophysiology of dreaming may have been a preadaptation for the evolution of hominid consciousness. Dreaming locates the dreamer in emotionally salient social space, a trait possibly derived from hippocampal spatial mapping. This skill in self-imaging and location can be correlated with the broader social brain hypothesis. Dreaming is thus expected to share significant features with consciousness, symbolization, and cognitive mechanisms pertaining to culture; and it is shown to do so. Rival models of consciousness and dream function are compared and assessed, and Flanagan's assertion that dreaming is epiphenomenal is challenged.

The relationships between memory systems and sleep stages

Geraldin Rauchs — 2005-05-23T08:53:36-00:00

Journal of Sleep Research, Vol. 14, No. 2. (June 2005), pp. 123-140.

Memory consolidation in sleep; dream or reality.

RP Vertes — 2008-01-29T13:34:10-00:00

Neuron, Vol. 44, No. 1. (30 September 2004), pp. 135-148.

We discuss several lines of evidence refuting the hypothesis that procedural or declarative memories are processed/consolidated in sleep. One of the strongest arguments against a role for sleep in declarative memory involves the demonstration that the marked suppression or elimination of REM sleep in subjects on antidepressant drugs or with brainstem lesions produces no detrimental effects on cognition. Procedural memory, like declarative memory, undergoes a slow, time-dependent period of consolidation. A process has recently been described wherein performance on some procedural tasks improves with the mere passage of time and has been termed "enhancement." Some studies, but not others, have reported that the consolidation/enhancement of perceptual and motor skills is dependent on sleep. We suggest that consolidation or enhancement, initiated in waking with task acquisition, could in some instances extend to sleep, but sleep would serve no unique role in these processes. In sum, there is no compelling evidence to support a relationship between sleep and memory consolidation.

The role of sleep in learning and memory.

P Maquet — 2008-01-10T09:19:35-00:00

Science, Vol. 294, No. 5544. (2 November 2001), pp. 1048-1052.

Sleep has been implicated in the plastic cerebral changes that underlie learning and memory. Indications that sleep participates in the consolidation of fresh memory traces come from a wide range of experimental observations. At the network level, reactivations during sleep of neuronal assemblies recently challenged by new environmental circumstances have been reported in different experimental designs. These neuronal assemblies are proposed to be involved in the processing of memory traces during sleep. However, despite this rapidly growing body of experimental data, evidence for the influence of sleep discharge patterns on memory traces remains fragmentary. The underlying role of sleep in learning and memory has yet to be precisely characterized.

Sleeping brain, learning brain. The role of sleep for memory systems.

P Peigneux — 2008-01-29T13:21:47-00:00

Neuroreport, Vol. 12, No. 18. (21 December 2001)

The hypothesis that sleep participates in the consolidation of recent memory traces has been investigated using four main paradigms: (1) effects of post-training sleep deprivation on memory consolidation, (2) effects of learning on post-training sleep, (3) effects of within sleep stimulation on the sleep pattern and on overnight memories, and (4) re-expression of behavior-specific neural patterns during post-training sleep. These studies convincingly support the idea that sleep is deeply involved in memory functions in humans and animals. However, the available data still remain too scarce to confirm or reject unequivocally the recently upheld hypothesis that consolidations of non-declarative and declarative memories are respectively dependent upon REM and NREM sleep processes.

Monitoring and control processes in the strategic regulation of memory accuracy.

A Koriat — 2005-10-30T04:10:57-00:00

Psychol Rev, Vol. 103, No. 3. (July 1996), pp. 490-517.

When people are allowed freedom to volunteer or withhold information, they can enhance the accuracy of their memory reports substantially relative to forced-report performance. A theoretical framework addressing the strategic regulation of memory reporting is put forward that delineates the mediating role of metamemorial monitoring and control processes. Although the enhancement of memory accuracy is generally accompanied by a reduction in memory quantity, experimental and simulation results indicate that both of these effects depend critically on (a) accuracy incentive and (b) monitoring effectiveness. The results are discussed with regard to the contribution of meta-memory processes to memory performance, and a general methodology is proposed that incorporates these processes into the assessment of memory-accuracy and memory-quantity performance.

The Role of Sleep in Declarative Memory Consolidation--Direct Evidence by Intracranial EEG

Nikolai Axmacher — 2007-10-18T01:42:01-00:00

Cereb. Cortex (14 June 2007), bhm084.

Two step theories of memory formation assume that an initial learning phase is followed by a consolidation stage. Memory consolidation has been suggested to occur predominantly during sleep. Very recent findings, however, suggest that important steps in memory consolidation occur also during waking state but may become saturated after some time awake. Sleep, in this model, specifically favors restoration of synaptic plasticity and accelerated memory consolidation while asleep and briefly afterwards. To distinguish between these different views, we recorded intracranial electroencephalograms from the hippocampus and rhinal cortex of human subjects while they retrieved information acquired either before or after a "nap" in the afternoon or on a control day without nap. Reaction times, hippocampal event-related potentials, and oscillatory gamma activity indicated a temporal gradient of hippocampal involvement in information retrieval on the control day, suggesting hippocampal-neocortical information transfer during waking state. On the day with nap, retrieval of recent items that were encoded briefly after the nap did not involve the hippocampus to a higher degree than retrieval of items encoded before the nap. These results suggest that sleep facilitates rapid processing through the hippocampus but is not necessary for information transfer into the neocortex per se. 10.1093/cercor/bhm084