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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.
Gava et al. explore the organization of neuronal co-activity in hippocampus from a graph theoretical perspective to report how new associative memories integrate into the network and restructure the neural patterns representing prior memories.
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.
By probing the dependence on learning history or motivational significance of stimuli, Sharpe and colleagues reveal previously uncharacterized contributions of lateral hypothalamus GABA neurons to associative learning.
Blum et al. performed single-nucleus RNA sequencing of the adult mouse spinal cord. This analysis revealed heterogeneity in the autonomic and skeletal motor systems and provides a resource to study motor neurons in health and disease.
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.
Good–bad binary classifications fail to describe reactive astrocytes in CNS disorders. Here, 81 researchers reach consensus on widespread misconceptions and provide definitions and recommendations for future research on reactive astrocytes.
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.
This study defined spatial gene expression in the human dorsolateral prefrontal cortex. It reveals layer-enriched expression of genes associated with schizophrenia and autism, highlighting the clinical relevance of spatially defined expression.
A new study discovered that ventral pallidal neurons projecting back to the nucleus accumbens promote consumption. The findings call into question the accepted direction of information flow through the ventral basal ganglia and open new avenues for studying how consumption is regulated in proportion to subjective value.
Leslie Gail Ungerleider, a distinguished experimental psychologist and neuroscientist, previously Chief of the Laboratory of Brain and Cognition at the National Institute of Mental Health, died suddenly on 11 December 2020. Friends, family, colleagues, and trainees all the world over mourn her passing, but also celebrate her life and extraordinary achievements.
Boulting et al. profile activity-dependent gene expression and regulatory elements in human induced pluripotent stem cell-derived GABAergic neurons and uncover a possible role for calcium-responsive gene promoters of these neurons in autism risk.
Fibrotic scarring after inflammation is well-characterized in peripheral tissues, but its role in the CNS is less clear. A new study shows that local proliferation of CNS fibroblasts drives fibrotic scar formation in response to circulating inflammatory cell infiltration in a model of multiple sclerosis, which may limit repair.
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.