Neurons take a break during slow-wave sleep

The Human K-Complex Represents an Isolated Cortical Down-State
Science 22 May 2009:Vol. 324. no. 5930, pp. 1084 - 1087

The electroencephalogram (EEG) is a mainstay of clinical neurology and is tightly correlated with brain function, but the specific currents generating human EEG elements remain poorly specified because of a lack of microphysiological recordings. The largest event in healthy human EEGs is the K-complex (KC), which occurs in slow-wave sleep. Here, we show that KCs are generated in widespread cortical areas by outward dendritic currents in the middle and upper cortical layers, accompanied by decreased broadband EEG power and decreased neuronal firing, which demonstrate a steep decline in network activity. Thus, KCs are isolated "down-states," a fundamental cortico-thalamic processing mode already characterized in animals. This correspondence is compatible with proposed contributions of the KC to sleep preservation and memory consolidation.

Face recognition memory

Does sleep really influence face recognition memory?
PLoS ONE 2009;4(5):e5496.
Sheth BR, Nguyen N, Janvelyan D.

Mounting evidence implicates sleep in the consolidation of various kinds of memories. We investigated the effect of sleep on memory for face identity, a declarative form of memory that is indispensable for nearly all social interaction. In the acquisition phase, observers viewed faces that they were required to remember over a variable retention period (0-36 hours). In the test phase, observers viewed intermixed old and new faces and judged seeing each before. Participants were classified according to acquisition and test times into seven groups. Memory strength (d') and response bias (c) were evaluated. Substantial time spent awake (12 hours or more) during the retention period impaired face recognition memory evaluated at test, whereas sleep per se during the retention period did little to enhance the memory. Wakefulness during retention also led to a tightening of the decision criterion. Our findings suggest that sleep passively and transiently shelters face recognition memory from waking interference (exposure) but does not actively aid in its long-term consolidation.

Exercise and sleep deprivation

The impact of 100 hours of exercise and sleep deprivation on cognitive function and physical capacities.
J Sports Sci. 2009 May 11:1-10.
Lucas SJ, Anson JG, Palmer CD, Hellemans IJ, Cotter JD.

In this study, we examined the effect of 96-125 h of competitive exercise on cognitive and physical performance. Cognitive performance was assessed using the Stroop test (n = 9) before, during, and after the 2003 Southern Traverse adventure race. Strength (MVC) and strength endurance (time to failure at 70% current MVC) of the knee extensor and elbow flexor muscles were assessed before and after racing. Changes in vertical jump (n = 24) and 30-s Wingate performance (n = 27) were assessed in a different group of athletes. Complex response times were affected by the race (16% slower), although not significantly so (P = 0.18), and were dependent on exercise intensity (less so at 50% peak power output after racing). Reduction of strength (P < 0.05) of the legs (17%) and arms (11%) was equivalent (P = 0.17). Reductions in strength endurance were inconsistent (legs 18%, P = 0.09; arms 13%, P = 0.40), but were equivalent between limbs (P = 0.80). Similar reductions were observed in jump height (-8 +/- 9%, P < 0.01) and Wingate peak power (-7 +/- 15%, P = 0.04), mean power (-7 +/- 11%, P < 0.01), and end power (-10 +/- 11%, P < 0.01). We concluded that: moderate-intensity exercise may help complex decision making during sustained stress; functional performance was modestly impacted, and the upper and lower limbs were affected similarly despite being used disproportionately.

Multiple genes and multiple phenotypes

Sleep and circadian rhythm disturbances: multiple genes and multiple phenotypes.
Curr Opin Genet Dev
Wulff K, Porcheret K, Cussans E, Foster RG

Sleep is regulated by two broad mechanisms: the circadian system, which generates 24-h rhythms of sleep propensity and a wake-dependent homeostatic sleep process whereby sleep pressure increases during wake and dissipates during sleep. These, in turn, regulate multiple brain structures and neurotransmitter systems. In view of the complexity of sleep it is not surprising that there is considerable variation between individuals in both sleep timing and propensity. Furthermore, marked abnormalities in sleep are commonly encountered in psychiatric and neurodegenerative disorders. Teasing apart the genetic versus environmental contributions to normal and abnormal sleep is complex. Here we attempt to summarise what recent progress has been made, and what will be needed in the future to gain a more complete understanding of this fundamental aspect of physiology.