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Duncan and colleagues link specific human brain cell types to schizophrenia and other complex brain phenotypes, providing mechanistic insights and a cellular taxonomy for psychiatric disorders.
Our brains evolved to help us rapidly learn new things. But anyone who has put in hours of practice to perfect their tennis serve, only to reach a plateau, can attest that our brains aren’t infinitely flexible. New work shows that patterns of neural activity over time — the temporal dynamics of neural populations — cannot change rapidly, suggesting that neural activity dynamics may both reflect and constrain how the brain performs computations.
Neuronal micronuclei are transferred to microglia during the early postnatal period, which leads to altered microglial morphology and transcriptomic signatures, suggesting that these micronuclei may act as mediators that control microglial characteristics.
Oby, Degenhart, Grigsby and colleagues used a brain–computer interface to challenge monkeys to override their natural time courses of neural activity. They found the time courses to be highly robust, suggestive of network-level computational mechanisms.
Groos et al. show that lateral habenula activity reflects individual risk preference before action selection. This activity is modulated by behavior-relevant synaptic input from the medial hypothalamus capable of glutamate and GABA co-release.
Multimodal transcriptomics unveil the molecular dynamics of neural stem cells and their surrounding niche in the aging mouse hippocampus and provide a resource to understand age-related molecular changes.
Nguyen et al. identify TDP-43 and METTL3 as key regulators of disrupted RNA splicing in Huntington’s disease, offering insight into how TDP-43 mislocalization and aberrant m6A RNA modification and localization relate to disease pathogenesis.
The brain uses different valuation schemes across contexts. Elston and Wallis show this is supported by hippocampal encoding of context that is broadcast to prefrontal value subcircuits via theta synchronization.
Hehlert et al. report that the gating spring that pulls open mechanosensitive NOMPC channels is not their helical ankyrin tether, but instead an elastic hinge that suspends that tether on the channel gate.
This article discusses a puzzling issue in brain pathology: why brain-resident microglia are insufficient for protection, and why myeloid cells are needed from the periphery. Several strategies are proposed to enhance their recruitment to the brain.
Microglia are proposed to have a role in brain development through synaptic engulfment and paracrine signaling. O’Keeffe et al. show that certain neurodevelopmental processes attributed to microglia can proceed normally even in the absence of these cells.
Mice react differently to others’ stress depending on their own past experience of the same (but not different) stress. Corticotropin-releasing factor (CRF) neuron activity in the medial prefrontal cortex (mPFC) specifically modulates the influence of affective past experience on emotional reactions to others, which was estrus-dependent in females and dominance-dependent in males.
Simultaneous intracranial electroencephalographic recordings from individuals playing a dynamic cooperation game reveal unique neural profiles of high-gamma intra-brain activity and inter-brain synchronization in the temporoparietal junction and the amygdala.
This study shows that cerebellar Bergmann glia process noxious stimuli by integrating signals from the locus coeruleus. This mechanism modulates pain-related behaviors. These findings provide insight into cerebellar involvement in pain processing.
Individual variability in behavior is influenced by social identities. Here, Dhamala et al. discuss the need to incorporate social identities in neuroimaging studies of behavior and explore how to foster inclusivity in research.
Mice expressing humanized mutant tau exhibit synaptic loss and behavioral abnormalities in the absence of abnormal tau conformers, suggesting that hyperphosphorylated tau can be pathological, at least in tauopathies caused by tau isoform imbalance.
