Innate Immunity Promotes Sleep through Epidermal Antimicrobial Peptides.

Wounding and infection trigger a protective innate immune response that includes the production of antimicrobial peptides in the affected tissue as well as increased sleep. Little is known, however, how peripheral wounds or innate immunity signal to the nervous system to increase sleep. We found that, during C.

A wake-active locomotion circuit depolarizes a sleep-active neuron to switch on sleep.

Sleep-active neurons depolarize during sleep to suppress wakefulness circuits. Wake-active wake-promoting neurons in turn shut down sleep-active neurons, thus forming a bipartite flip-flop switch. However, how sleep is switched on is unclear because it is not known how wakefulness is translated into sleep-active neuron depolarization when the system is set to sleep.

Sleep Counteracts Aging Phenotypes to Survive Starvation-Induced Developmental Arrest in C. elegans.

Sleep is ancient and fulfills higher brain functions as well as basic vital processes. Little is known about how sleep emerged in evolution and what essential functions it was selected for. Here, we investigated sleep in Caenorhabditis elegans across developmental stages and physiological conditions to find out when and how sleep in a simple animal becomes essential for survival.

Neuroplastic effects of transcranial near-infrared stimulation (tNIRS) on the motor cortex.

Near-infrared light stimulation of the brain has been claimed to improve deficits caused by traumatic brain injury and stroke. Here, we exploit the effect of transcranial near-infrared stimulation (tNIRS) as a tool to modulate cortical excitability in the healthy human brain. tNIRS was applied at a wavelength of 810 nm for 10 min over the hand area of the primary motor cortex (M1).