Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Gordon et al. use genome-wide unbiased approaches to show that human cerebral cortical organoids, when cultured for many months, start to resemble stages of postnatal brain development, with a timeline that parallels in vivo development.
Examination of neural activity reveals that performing a rapid sequence of actions depends not upon fusing those actions into a holistic unit, but upon the ability of motor cortex to swiftly prepare the next action while the present unfolds.
Oxidized phosphatidylcholines found in MS lesions are not just markers of oxidative stress but are also promoters of demyelination and axon injury. Microglia suppress oxidized-phosphatidylcholine-mediated neurodegeneration by phagocytosis through TREM2.
Bonapersona and colleagues describe how historical control data can be used to improve statistical power while reducing the number of animals required in experiments. They present an open-source tool, RePAIR, that can be used to apply this approach.
Vast networks of capillaries feed the brain. Hartmann et al. show that pericyte contractility is critical for maintenance of enduring capillary tone, which sets an optimized rate and distribution of blood flow through brain capillary networks.
This study shows that a subpopulation of astrocytes in the central amygdala (CeA) expresses the oxytocin receptor (OTR) and that OTR activation in astrocytes underlies the anxiolytic and positive reinforcement effects of oxytocin in the CeA.
Sharpe et al. find that prior reward-learning experience can prime reward circuits to encode fear memories. This suggests prior experience can shape the way we learn, opening the neural boundaries for learning about particular types of information.
Guttikonda et al. engineered a human pluripotent stem cell-derived tri-culture system containing microglia, astrocytes, and neurons. This system recapitulates cell-type-specific inflammatory signaling in an in vitro model of Alzheimer’s disease.
Dorrier et al. identified fibrotic scarring in a mouse model of multiple sclerosis that arises from the proliferation of fibroblasts in the meninges and surrounding blood vessels, and determine that reducing scarring decreases motor symptom severity.
Zhang et al. show in mice that the medial preoptic area antagonistically regulates stress-induced anxiety and parental behaviors, coordinated by opposing roles of its glutamatergic and GABAergic neurons through their competitive interactions.
Paredes et al. identify bidirectional crosstalk between the neural and the vascular compartment in the developing CNS required for oligodendrocyte precursor cell specification and mediated by an angiopoietin1–Tie2–TGFß1 signaling axis.
Synapse loss is prominent in the cortex in multiple sclerosis (MS). In a cortical MS model, Jafari et al. show that phagocytes remove synapses by engulfment, which is triggered by local calcium accumulations and prevented by blocking colony-stimulating factor 1 signaling.
Two-photon photostimulation and imaging of a cortical short-term memory circuit reveal intercalated modules that can independently maintain memory. The modules are defined by connectivity between neurons with similar task-related tuning.
Inhibition of nucleus accumbens neurons is crucial for reward consumption. Vachez, Tooley et al. characterize arkypallidal neurons in the ventral pallidum that inhibit accumbal neurons to sustain reward consumption in a value-dependent manner.
This study shows how different myeloid cell types contribute to damage and repair following cerebrovascular injury, a pathology common to many central nervous system disorders, and offers new therapeutic opportunities to improve clinical outcomes.
Sherman et al. describe the contribution of mosaic copy number variants (mCNVs) to the risk of autism spectrum disorder (ASD). Probands with ASD carry a significant burden of mCNVs relative to their unaffected siblings.
Zhu et al. discover that in human brain there is widespread anatomic distribution of low-frequency somatic, mosaic L1 insertions, using deep whole-genome sequencing of neuronal and glial fractions and machine-learning analysis.
Rodin and Dou et al. characterized genome-wide somatic mutation in autistic and control brains, revealing that even unaffected individuals may possess dozens of brain somatic mutations and providing insight into the role of somatic mutation in autism.