Volume 19 Issue 6, June 2018

Different 3′ untranslated regions of mRNA transcripts are associated with differences in mRNA localization, translation, stability and activity-dependent changes in expression.

In mice, aggression is regulated by the circadian suprachiasmatic nucleus through at least two neural pathways.

A new study suggests an evolutionary mechanism — involving abnormal spindle-like microcephaly-associated protein — that, in part, underlies cerebral cortical expansion.

Elevated maternal IL-6 in the maternal circulation can enter the fetus via the maternal—placental—fetal route and alter neurodevelopmental processes, with potentially wide-ranging effects on brain function later in life.

Distinct output pathways of the nucleus accumbens mediate the opposing effects of context on relapse to alcohol seeking.

In the mouse postnatal hippocampus, microglia trim presynaptic structures by a partial phagocytic process termed trogocytosis and remodel postsynaptic structures.

Peripheral axon injury initiates a regenerative response that is absent in CNS axons. Mahar and Cavalli describe the mechanisms that initiate and coordinate the programme of transcriptional and epigenetic changes that enable axon regeneration in the peripheral nervous system.

The basal ganglia and the cerebellum were thought to communicate via the cerebral cortex. In this Review, Andreea Bostan and Peter Strick discuss findings indicating that these subcortical areas are in fact interconnected and, along with the cerebral cortex, form an integrated network.

Breathing is a crucial yet surprisingly complex behaviour. Del Negro, Funk and Feldman describe the neural mechanisms underlying different phases of the breathing cycle, and how breathing affects, and is affected by, emotion, cognition and other behaviours.

The neurodevelopmental disorder Rett syndrome is caused by a deficiency in methyl-CpG-binding protein 2 (MeCP2). Ip, Mellios and Sur describe the many functions of MeCP2 and the effects of MeCP2 loss on gene expression, excitation–inhibition balance and activity-dependent plasticity.