Reviews & Analysis

A new study sheds light on how sensitivity to communication sounds is established in the brain. Juvenile finches raised with tutors of either the same or different species always learned the tutors’ songs. Cortical neurons developed selectivity for the learned song by tuning for its secondary acoustic features.

Chronic pain is associated with anxio-depressive comorbidities, but the neuroanatomical substrates remain unknown. A specific serotonergic pathway from the dorsal raphe nucleus to the lateral habenula via the central amygdala is now uncovered as a key neural circuit governing comorbid depressive symptoms in chronic pain.

While we sleep, the brain replays memories of our experiences during the day. In this review, Klinzing et al. provide a concise overview of how the sleeping brain transforms and builds persisting memories through this process.

Repeat-associated non-AUG (RAN) translation generates toxic repeat proteins from pathological repeat expansions found in certain neurodegenerative disorders, including amyotrophic lateral sclerosis and frontotemporal dementia. How to suppress RAN translation has so far been unknown. A new study now reports a selective regulator of RAN translation identified in a genetic screen in yeast.

Misfolded protein aggregates are a classical hallmark of many neurodegenerative diseases. By combining a mouse model of misfolded protein injection and a brain network model of misfolded protein diffusion, a study now finds a strong link between the stereotypical spreading patterns of neurodegeneration, protein expression and anatomical connectivity.

Mosquito-borne virus infections, such as West Nile and Zika, have debilitating cognitive effects that persist despite recovery from encephalitis. Garber et al. identify mechanisms by which antiviral T cell persistence after recovery from infection leads to impairments in cognition via virus-specific mediation of microglial synapse elimination.

Shahmoradian and colleagues report that the structure of Lewy bodies in Parkinson’s disease consists of α-synuclein and lipid vesicle clusters instead of the long-assumed amyloid fibril core. This finding has implications for our understanding of the underlying pathogenesis of synucleinopathies.

The creation of a murine Cre driver specific to CNS capillary pericytes has opened a major bottleneck in brain microvascular research. Using this tool, pericyte loss in the adult brain is shown to induce neuronal loss due to concurrent microcirculatory failure and depletion of the protective trophic factor pleiotrophin.

A new study by Owen et al. shows that widely used optogenetic light delivery can heat brain tissue and produce changes in neural activity and behavior in the absence of opsins. How will this finding influence experimental design in the optical age of neuroscience?

Selecting the most rewarding action and performing it accurately are two separable brain functions that are thought to rely upon different neural systems. New evidence suggests that the cerebellum could learn to do both.

How to know when to hunt or when to lay low? Surprisingly, new research shows that activity in the medial zona incerta specifically initiates predation in the mouse. The medial zona incerta integrates visual motion and tactile stimulation sent from the intermediate superior colliculus to motivate hunting.

The CNS harbors distinct subsets of macrophages, including parenchymal microglia and macrophages residing at border regions (for example, meninges and the choroid plexus). In this issue of Nature Neuroscience, Van Hove and colleagues elegantly demonstrate the diversity and dynamics of non-parenchymal macrophages and identify a unique microglial subtype within the choroid plexus.

Using light-activated ion channels to stimulate sensory and motivational pathways, Vetere and colleagues constructed fully artificial memories in mice. Mice preferred or avoided an odor they had never smelled before, depending on the pattern of stimulation.

DNA damage or cellular stresses can induce senescence, and increased senescence with aging contributes to age-associated tissue damage, inflammation and disease. Zheng and colleagues report increased senescent oligodendrocyte progenitor cells around amyloid plaques. Therapeutically eliminating these senescent cells may influence the onset and progression of Alzheimer’s disease pathology.

Robust conclusions require rigorous statistics. In 2009 a seminal paper described the dangers and prevalence of double-dipping in neuroscience. Ten years on, I consider progress toward statistical rigor in neuroimaging.

A new study reveals an unexpected mechanism underlying behavioral abnormalities in the neurodevelopmental disorder Williams syndrome. A deficit in myelination, resulting from the deletion of a Williams syndrome-associated gene in forebrain excitatory neurons, causes hypersociability by impairing action potential conduction. Accordingly, rescuing myelination or conduction normalizes this behavior.

Noninvasive delivery of alternating electrical currents to temporal and prefrontal brain regions improves working memory and reverses age-related changes in brain dynamics in the elderly, report Reinhart and Nguyen in this issue of Nature Neuroscience. They also report a similar effect in young adults with poor working memory performance.

The ventrolateral and medial orbitofrontal cortices are involved in selecting actions based on the value of expected outcomes. Malvaez and colleagues reveal that these brain regions are specialized in value encoding (ventrolateral orbitofrontal cortices) versus value memory retrieval (medial orbitofrontal cortices) and that they interact with the basolateral amygdala to orchestrate goal-oriented reward-seeking.

When choosing whether to act altruistically, people may compare the current option to an idiosyncratic ideal. Prosocial individuals seem to represent deviations from that ideal in the amygdala, but selfish individuals do not. Oxytocin administration makes selfish individuals look more like prosocial individuals, behaviorally and neurally.

The cell of origin for malignant brain tumors remains uncertain, but de-differentiation from mature cells in the CNS has always been considered a strong possibility. In this issue of Nature Neuroscience, Alcantara Llaguno and colleagues report that differentiated neurons resist transformation by glioblastoma-associated mutations, pointing to neural stem cells or immature progenitors as the most likely cells of origin for these tumors, rather than cells of a relatively mature neuronal lineage.