Articles in 2018

A dynamic mRNA modification promotes axon regeneration in injured peripheral sensory neurons.

The changes in spinal cord excitability proposed to drive neuropathic pain have been linked to alterations in microglial function. Inoue and Tsuda describe our current understanding of the molecular mechanisms involved and consider implications for therapeutic approaches to chronic pain.

'Social place cells' of the dorsal hippocampal CA1 region in bats and in rats encode the position of an observed conspecific.

Human-gained enhancers (regulatory elements in the human genome that are more active in the human lineage) are shown to regulate progenitor proliferation in the outer subventricular zone, an area that is substantially larger in humans compared with other primates.

Two recent papers reveal that the activity-regulated cytoskeleton-associated proteins ARC andDrosophila melanogasterdArc1 auto-assemble into mRNA-containing, virus-like capsids that are released by neurons in exosomal vesicles and that can be endocytosed at the postsynaptic compartment.

When mice explore a new context, neurons in the locus coeruleus that project to hippocampal regions CA3 enable the learning of the new environment.

Microglial surveillance of the brain is dependent on maintenance of microglia membrane potential by the K⁺channel THIK1, which is potentiated by ATP released at sites of tissue injury acting on P2Y12 receptors.

Amyloid-β (Aβ)-induced proteotoxicity is linked to a mitochondrial stress response that may be conserved across species, and promoting mitochondrial proteostasis counteracts Aβ aggregation in worms and an Alzheimer disease mouse model.

Mitochondria may be actively recruited to presynapses to supply energy, buffer calcium and, potentially, fulfil other functions. In this Review, Devine and Kittler examine the importance of this presynaptic population of mitochondria in the maintenance of neuronal homeostasis and how dysfunctional presynaptic mitochondria might contribute to neurodegenerative diseases.

Eating patterns in modern societies often preclude the metabolic switch from utilization of glucose to ketones as a cellular energy source. In this Review, Mattson and colleagues discuss how intermittent metabolic switching impacts brain function and vulnerability to injury and disease.

Although leptin administration decreases food intake and body weight in lean mice, it has no effect in obese mice. In this Review, Pan and Myers discuss how leptin action becomes dysfunctional in obesity and suggest that elevated leptin levels promote processes that limit leptin action.

During low-vigilance states, thalamic neurons exhibit diverse rhythmic activities that contribute to specific parts of the electroencephalogram rhythm. In this perspective, Crunelli and colleagues propose that thalamic oscillations of these low-vigilance states also have a plasticity function that modifies the strength of excitatory and inhibitory synapses in local neuronal assemblies.