News & Comment

Neurons exhibiting synaptic upscaling or downscaling in response to decreases or increases in activity, respectively, show changes in protein expression that depend on the duration and the polarity of the change.

Upregulated bursting activity in the lateral habenula is associated with depression-like behaviours in rats and mice, and depends on NMDA receptors, T-type voltage-sensitive calcium channels and the astrocytic inwardly rectifying potassium channel KIR4.1.

A population of 'anxiety cells' that encode anxiogenic information and drive avoidance behaviour is identified in the mouse hippocampus.

In mice, consumption of a high-salt diet induces accumulation of T helper 17 lymphocytes in the gut, leading to a rise in plasma interleukin-17 levels as well as neurovascular dysfunction and cognitive deficits.

Two studies characterize inputs to the periaqueductal grey that regulate hunting behaviour in mice.

Axons of striatal dopaminergic neurons are shown to release dopamine in a RIM-dependent manner and with a high release probability from axonal active zone-like structures.

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

'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.