Ouellette et al. report that a 16p11.2 deletion induces a bioenergetic failure in brain endothelial cells. Activation of purinergic signaling via P2Y2 receptors restored endothelial function and improved behaviors in mice carrying a 16p11.2 deletion. Targeting endothelial metabolism and purinergic signaling may thus represent a promising therapeutic avenue for autism.

Qi and colleagues show that TMEM119 constitutively restrains microglial phagocytosis by sequestering tankyrase from axin and thereby limiting APC-driven actin assembly. Genetic TMEM119 ablation or interference of TMEM119-tankyrase binding by a brain-penetrant peptide enhances synapse elimination and attenuates established fear memory, opening a new way for pharmacological memory manipulation.

Chen et al. show that SCN2A protein-truncating variants disrupt cortico-striatal circuitry while increasing neuronal excitability in human brain assembloids. CAV-2-mediated SCN2A restoration mitigates intrinsic hyperexcitability and circuit deficits, supporting targeted gene replacement as a potential therapeutic strategy for SCN2A-related neurodevelopmental disorders.

Weitzman et al. show that genetic variation at the MAPT region differs across ancestries, revealing a previously unknown haplotype that challenges widely used genetic markers. Their findings demonstrate how ancestry shapes gene regulation and highlight the importance of diverse populations for understanding neurodegenerative disease risk.

Li et al. present OpenFISH, an open, cost-effective imaging-based spatial transcriptomics platform with single-cell resolution that enables same-section MALDI-MSI integration. OpenFISH maps inflammatory TE responses and Reeler-associated patterning changes, while its multimodal workflow resolves cell-type-associated metabolic patterns in the nervous system and candidate metabolic changes in the 5xFAD brain.

Khan, Clement et al. show that subjects undergoing removal of cervical lymph nodes presented an elevated risk for cognitive impairment. The disruption of brain lymphatic clearance triggers metabolic and oxidative stress, which is conducive to neuronal damage. These findings reveal a connection between impaired metabolic waste disposal and cognitive impairment.

Researchers often have the goal of estimating aperiodic signal changes across time. Here, Cellier et al. present a series of recommendations for ensuring that aperiodic parameterization algorithms are optimized for resolving spectral EEG activity over short time windows.

Emmerson et al. demonstrate that the CXCR3-CXCL10 chemokine signaling pathway is important for brain-infiltrating T cells in tau-mediated neurodegeneration. Blocking CXCR3 reduces T cell entry and protects against neuronal loss, thus identifying peripheral immune targeting as a promising niche therapeutic strategy for tauopathies.

Dorsal horn Grpr+ neurons are widely considered itch specific, but Noh et al. reveal they are also required for chronic pain. The population comprises two closely related transcriptomic subtypes: the Grpr+Tac1– subtype mediates chemical itch, and the Grpr+Tac1+ subtype serves as a critical node for mechanical hypersensitivity across inflammatory, neuropathic, and polyneuropathic injuries.

Dai et al. identify a microglial osteopontin (SPP1)-integrin β1 feedback program that sustains mechanical allodynia after thalamic hemorrhage. Genetic and pharmacological experiments place CC-chemokine signaling downstream of osteopontin and show that broad CC-chemokine inhibition reduces both allodynia and peri-lesional neuronal hyperexcitability.

Cornford et al. show that exponentiated gradient (EG) learning, which updates synapses multiplicatively, matches gradient descent on cognitive tasks while respecting Dale’s law and producing brain-like log-normal weight distributions. EG-trained networks better withstand synaptic pruning and learn more effectively when many inputs are task-irrelevant.

Hobel et al. describe a direct, functional projection from the basolateral amygdala to dorsolateral striatum. This sparse pathway modulates dorsolateral striatal activity, can prolong and augment sensory-evoked motor responses, and is overactive in a Sapap3 null mouse model of OCD, providing a route for limbic modulation of sensorimotor behavior.

Liu et al. identify a population of Lef1+ hypothalamic neurons that coordinates feeding and thermogenic adaptations to cold. Cold suppresses Kcnk2/TREK-1 function to enhance neuronal activity, revealing a molecular mechanism linking environmental temperature to neural and metabolic responses.

Comrie et al. show that the hippocampus flexibly represents different alternative possibilities—including paths ahead, behind, and far away—to meet distinct cognitive demands related to decision-making and learning. Their results demonstrate that the brain can selectively sample possibilities relevant to current needs.

Chen et al. identify anterior zona incerta aZIT neurons as key drivers of compulsive binge eating. Intermittent high-fat-diet exposure increases GABAergic aZIT neuronal excitability, thus enhancing mesolimbic dopamine signaling through direct and indirect circuits and driving aversion-resistant compulsive binge eating. Nrsn2 marks the aZI neuronal population required for BED development.

Qu et al. link emerging brain vulnerability during female midlife to molecular communication between peripheral organs and the brain. They trace this connection to miR-10a-5p-γCaMKII signaling, revealing a cross-organ dimension of cognitive aging.

Zhang et al. show that NFIs act as evolutionarily conserved global temporal regulators and bidirectionally control the pace of RGP lineage progression and consequently progeny output during neocortical development, providing direct insights into NFI mutation-associated human brain malformations.

This review by Summerfield and Stachenfeld surveys how the dialog between neuroscience and AI research has evolved over the past decade. They highlight continued opportunities for synergy between these disciplines.

Both inhibitory inputs to the mPOA and mPOA activation are required for male mating, but how inhibition contributes to neuronal activity during mounting remains unclear. Zhang et al. identify T-type calcium channel-mediated post-inhibitory rebound firing in the mPOA as a mechanism that converts inhibition into excitation to facilitate mount initiation.

Essner, Ruda, and colleagues use large-scale, multi-day calcium imaging in awake and anesthetized mice to characterize how brainstem lateral parabrachial neurons encode body signals. Largely distinct, spatially organized groups of neurons in this interoceptive hub preferentially respond to oral or post-ingestive feeding signals, locomotion, arousal, and/or feedback from cortex.

Chericoni et al. show that neurons in the human hippocampus track the positions of multiple agents in a simple pursuit-based video game. They identified place codes for each agent and for gaze. The co...

Li et al. report a positive correlation between local sympathetic inputs and the severity of liver fibrosis in patients, a phenomenon that similarly occurs in a mouse disease model. Local sympathetic signals act via the α1B-adrenergic receptor to promote immune evasion of hepatic stellate cells from natural killer cells.

We identify the amygdalostriatal transition zone (ASt) as a genetically distinct region that plays a previously unappreciated role in conditioned fear responses. We find that ASt neurons show sustained responses to shock-predictive cues and are both necessary and sufficient for the expression of defensive behaviors.

Kay, Levesley, et al. show that the strongest genetic modifier of Huntington’s disease (HD), a loss of interruption in the causative HTT CAG repeat, increases somatic expansion in neurons that are selectively lost in the disease. Their findings suggest that genetic changes in disease-causing repeats can modify cell-type-specific pathology.

Dai et al. identify stress-responsive neuropeptide Y receptor Y1-expressing neurons in the hypothalamic paraventricular nucleus that engage the dorsal vagal complex to suppress feeding and delay gastric emptying. Inhibiting this pathway alleviates these stress-induced responses, revealing a hypothalamic-brainstem circuit coordinating feeding and gastric function during acute stress.

Zhao et al. show that social information is represented in the nucleus accumbens and becomes unstable in a mouse model of autism. They further identify distinct contributions of D1- and D2-medium spiny neurons to social behavior and show that targeting these circuits can ameliorate social deficits.

Cohen and Gong provide a practical guide to voltage imaging, covering voltage indicators, gene expression strategies, instrumentation, instrument control software, data analysis algorithms, and experimental protocols. Signal-to-noise ratios and sources of artifacts are discussed in detail.

Lin et al. developed an in vivo CRISPRi screening platform to map gene function directly in the mouse brain. Their genome-wide survey across neuronal types and ages reveals cell-type-specific and age-dependent vulnerabilities that are invisible to cell-based models, offering a functional view of the brain beyond gene expression atlases.

Chericoni et al. show that neurons in the human hippocampus track the positions of multiple agents in a simple pursuit-based video game. They identified place codes for each agent and for gaze. The codes were systematically related in a way that allowed generalization while preserving the ability to differentiate.

Uesaka et al. show that inhibitory brain circuits can suppress adult glioma growth by limiting tumor calcium signaling and downstream growth programs. The study reframes glioma progression as a balance between growth-promoting and growth-restraining neural inputs, suggesting that strengthening inhibitory tone may help control brain tumors.

Dong et al. identify a descending brainstem-to-spinal-cord circuit that drives widespread, opioid-resistant pain in mice. They show that glycine from this pathway acts as an excitatory signal by activating a specific type of NMDA receptor in the spinal cord, revealing a previously unknown mechanism for refractory tactile pain.

The findings suggest that astrocytes are much more than support cells for neurons – they also seem to directly regulate brain function.

Neuron by Cell Press | 65 followers on LinkedIn. Neuron, published by Cell Press, is one of the leading and most influential journals in neuroscience and a premier intellectual forum for the scientifi...

Cara, Guthman, et al. present neuro-seeER, an optical tool for monitoring how neurons respond dynamically to the hormone estrogen. By tracking these dynamics across the reproductive cycle in female mice, they reveal that individual neurons and different animals respond differently to hormone signals, thereby uncovering unexpected complexity in brain-hormone interactions.

Jarvie et al. identify two populations of parabrachial CGRP neurons, one that responds rapidly to appetitive signals during ingestion and the other that responds slowly to aversive visceral cues. The rapid CGRP neuron activation during ingestion is shown to be required for post-ingestive learning but not, as previously believed, satiety.

Nickolls et al. identify a clinical variant in PIEZO2 that impairs touch sensation and body awareness. By showing how this variant prevents PIEZO channels from opening and deforming under pressure, the study adds to our understanding of how specific PIEZO protein domains contribute to force-induced conformational changes.

Using fMRI and TMS, Liu et al. showed how the human brain learns whether outcomes are under one’s control. A circuit linking dorsomedial prefrontal cortex and dorsal raphe nucleus supports controllability estimates, while control estimates subsequently reshape teaching signals that guide learning.

Onasch, Miehl, et al. show how biologically inspired circuit mechanisms allow neuronal assemblies to form, remain stable, and be recruited in different contexts. Their model explains how these assemblies can support flexible learning and computation across brain areas while preserving previous representations.

How does language emerge from neural computations in the human brain? In stark contrast to symbolic theories of language, large language models demonstrate how the structures of language can be unified in a high-dimensional neural population code.

Astrocytes play essential roles in brain function by supporting neural circuits and cognition. Murali et al. find that the transcription factor NFIX is required to maintain astrocyte function in the thalamic reticular nucleus through region-specific control of GABA signaling. Altered astrocyte-neuron communication disrupts thalamocortical oscillations, impairing learning and memory.

Huszár, Kirsanov et al. show that hippocampal CA3 and CA1 neurons born on the same day form a functional subcircuit that encodes new memories. Spatial learning engaged convergent connectivity from embryonically related pyramidal neurons onto parvalbumin-expressing CA1 interneurons.

Jin et al. establish the win maze to study how mice decide to re-engage in competition after winning outcomes. They show that dominant males display stronger competition engagement, with dmPFC neural dynamics predicting future choices and mesocortical dopamine bidirectionally regulating engagement.