Articles in 2018

The core function of sleep remains unclear. In this Opinion, Anafi, Kayser and Raizen give an overview of sleep states in various phyla and propose that the original function of sleep was likely metabolic.

In addition to the central pacemaker, the mammalian brain contains additional circadian clocks. In this Review, Greco and Sassone–Corsi discuss how systemic homeostasis relies on the coordinated communication between these clocks.

Repetitive sensory input induces long-term potentiation of pyramidal cell synapses in mouse somatosensory cortex by activation of higher-order thalamic projections and disinhibition of local interneurons.

In this Opinion article, Hahn, Kumar and colleagues propose that synchrony- and oscillation-based communication between brain networks can be described by a common theoretical framework. They also suggest a mechanism for control of the flow of information in the brain through nesting of slow and fast oscillations.

Narcolepsy is a sleep disorder caused by selective loss of orexin-producing neurons. Scammell and colleagues describe the functions of orexin neurons and the effects of their loss and review evidence implicating the immune system in the pathogenesis of the disorder.

In mice, long-term potentiation of hippocampal–nucleus accumbens synapses is required for the formation of reward-related memories.

A study shows that application of spatiotemporally patterned epidural electrical stimulation alongside rehabilitation allowed individuals with spinal cord injury and severe locomotor deficits to walk with limited assistance.

Meal-associated thermogenesis in brown fat is triggered by the gut hormone secretin and signals to the brain to promote satiation in mice.

Maladaptive modulation of learning, memory and affect by opioids is linked to dysfunctional neurogenesis. In this Review, Kibaly and colleagues discuss this link and how strategies that target neurogenesis to rescue opioid-dependent learning, memory and affect impairments constitute future directions for anti-addiction therapies.

Two studies show that tau pathology drives the expression of complement molecules that in turn promote the phagocytosis of synapses and neuroinflammation.