Reviews & Analysis

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.

Astrocytes are emerging as causal or modulating factors in diverse neurological disorders. Two papers published in Nature Neuroscience in 2007 revealed astrocytes as causally contributing to motor neuron loss in amyotrophic lateral sclerosis, thereby challenging the longstanding neuron-centric view of neurodegenerative disease.

In this issue of Nature Neuroscience, Kim and colleagues report that corticotropin-releasing factor neurons in the paraventricular nucleus, known essential regulators of the neuroendocrine axis, encode the valence of environmental stimuli through a bidirectional strategy and modulate animals’ immediate behavioral responses.

Disproportionate reactions to unexpected stimuli and greater attention to perceived threat are cardinal symptoms of post-traumatic stress disorder. Computational psychiatry helps explain how these responses develop and result from abnormalities in learning and prediction during and after traumatic events.

Excessive synapse elimination during adolescence and early adulthood has long been hypothesized to underpin the emergence of schizophrenia. A new study reports that induced microglia-like cells derived from schizophrenia patients display increased synapse engulfment, which may be partly mediated by a genetic schizophrenia-risk variant.

Geneticists are pushing for ever-greater sample sizes to gain insight into the genetic variation that contributes to psychiatric disorders. Two new genome-wide association studies leverage this approach to provide broad, population-level perspectives on the genetic basis for major depressive disorder and the shared genetic risk that underlies multiple disorders.

Variability is a ubiquitous aspect of neural recordings. In an influential paper, Churchland et al. (2010) compiled data from many cortical areas to demonstrate that variability generally decreases upon presentation of a stimulus. What are the implications of this finding?

Experience unfolds continuously in time, but we remember discrete sequences of events. In this issue of Nature Neuroscience, Montchal et al. describe brain activity patterns that predict how well people remember precisely when recent events occurred. Converging evidence suggests that homologous neural machinery structures temporal representations in rats and people.

In 2008, Vyazovskiy et al. published a seminal study demonstrating that sleep induces a widespread downscaling of synapses that counters the synaptic upscaling that occurred during prior wakefulness. The study laid the groundwork for current research into the ‘where’ and ‘when’ of homeostatic neuronal network regulation during sleep.