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  • Duan Shumin and Sun Li's group published in Neuron on how slow-wave sleep prevents anxiety
    21 05
    The research team led by Prof. Li Sun and Prof. Shumin Duan has recently published an article titled Slow-wave sleep engages brainstem circuitry to prevent stress-induced anxiety in Neuron online on May 20th, 2026. This research identifies a specific brainstem circuit—the PZGABA→LPBCGRP→ovBNSTCrh pathway—through which slow-wave sleep (SWS) actively suppresses stress-induced anxiety.The anxiolytic benefit of sleep is not a passive consequence of global cortical synchrony but is actively orchestrated by this dedicated inhibitory circuit. Optogenetic induction of just 15 minutes of slow-wave sleep immediately after social defeat prevents the development of anxiety-like behaviors.Sleep is known to buffer stress, but whether it acts passively or through specific circuits has remained unclear. Using time-locked optogenetic SWS induction, cell-type-specific calcium recording, and circuit dissection, the authors show that sleep-active GABAergic neurons in the parafacial zone directly inhibit LPBCGRP alarm neurons, which in turn drive anxiety via ovBNSTCrh neurons. Blocking this PZ-LPB pathway during sleep abolishes its anxiolytic effect, whereas activating the pathway in awake animals induces anxiety. Notably, the LPB-ovBNST pathway, but not the LPB-basal forebrain pathway, selectively controls anxiety independent of arousal. These findings establish a causal circuit mechanism through which sleep actively resets emotional circuits, providing a neural target for treating anxiety disorders.Circuit-specific engagement of SWS as an endogenous anxiolytic against stress-induced anxiety Website: https://doi.org/10.1016/j.neuron.2026.04.041DUAN SHUMIN AND SUN LI'S RESEARCH GROUP: For the brain, sleep is not merely rest but an active state that shapes emotion and health. The group is dedicated to studying the neural circuitry linking sleep-wake states with emotional processing. They use cutting-edge techniques including in vivo multi-region fiber photometry, optogenetics, chemogenetics, EEG/EMG recording, and behavioral assays to dissect the circuit mechanisms through which sleep protects against stress-induced anxiety and depression.  
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  • Wang Hao’s Group Published in Nature Communications on High-Fat Food conditioned taste Aversion Memory
    11 05
    The research team led by Prof. Hao Wang recently published an article titled A midbrain circuit for high-fat-food induced conditioned taste aversion in Nature Communications online on April 18th, 2026. This study established a conditioned taste aversion (CTA) model using high-fat solid food and identified a midbrain neural circuit that mediates the formation and expression of aversive memory toward palatable food.Conditioned taste aversion is an evolutionarily conserved defense mechanism in which animals avoid foods previously associated with gastrointestinal discomfort. While previous studies mainly relied on liquid stimuli such as sucrose solutions, it remained unclear how the brain encodes aversive memories toward complex solid foods encountered in natural feeding conditions.To address this question, the researchers developed a novel mouse model pairing high-fat food consumption with lithium chloride (LiCl)-induced malaise. Through whole-brain activity screening, chemogenetics, optogenetics, and electrophysiological analysis, the team identified glutamatergic neurons in the midbrain raphe region (MRR) as a critical neural substrate for high-fat food aversion memory.The study showed that silencing MRR glutamatergic neurons prevented mice from forming aversive memory despite experiencing gastrointestinal discomfort. In contrast, artificial activation of these neurons was sufficient to induce avoidance of high-fat food even without malaise, suggesting that activation of the MRR circuit alone can generate an aversive memory signal.Further investigation revealed that glutamatergic neurons in the medial preoptic area (MPOA) provide direct upstream input to the MRR and transmit visceral malaise-related signals during aversion learning. The researchers also demonstrated that MRR neurons project through two functionally distinct downstream pathways. The MRR-medial septum (MS) pathway is required for memory encoding, whereas the MRR-lateral habenula (LHb) pathway mediates memory retrieval and behavioral expression of food avoidance.A midbrain circuit for high-fat-food induced conditioned taste aversionThis work reveals a cell type–specific neural circuit architecture underlying conditioned taste aversion toward solid food and establishes the MRR as a central hub linking visceral signals, memory processing, and feeding behavior. The findings provide new insight into the neural mechanisms of eating disorders associated with nausea and aversive feeding experiences, including anorexia, cachexia, and treatment-related appetite dysfunction.Website: https://doi.org/10.1038/s41467-026-72107-2WANG HAO’S RESEARCH GROUP: focus on the neural circuit mechanisms underlying innate behaviors and emotional regulation, including feeding, fear, and social behaviors. By combining cutting-edge approaches including circuit tracing, optogenetics, chemogenetics, electrophysiology, and behavioral analysis, the group investigates how the brain integrates sensory and internal state information to regulate adaptive behaviors and memory formation.
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  • LI Xiaoming’s group published in Cell on Rational Design of Gi-biased CB1 Agonist
    15 04
    The research team led by Professor Xiaoming Li, in collaboration with Professor Xiaowu Dong and Professor Yan Zhang, has recently published an article titled Rational Design of Gi-biased CB1 agonist with reduced side effects in Cell on April 13th, 2026. In this study, they developed Gi-biased CB1 receptor agonists that decouples therapeutic efficacy from adverse effects.The clinical use of cannabinoids for pain and emotional disorders is limited by their side effects, including addiction, cognitive impairment and tolerance. The therapeutic effects of CB1 agonists are primarily mediated by Gi/o protein signaling, whereas the recruitment of β-arrestin1 is associated with unwanted side effects. To decouple these pathways, the authors utilized previous structural insights into the CB1–β-arrestin1 complex to identify a specific steric clash within the receptor's binding pocket, which lead to a more deeply buried configuration to accommodate β-arrestin1 coupling.Based on this, they rationally designed compounds which favor Gi signaling. In mouse models of both chronic and acute pain, these Gi-biased agonists demonstrated potent analgesia comparable to traditional agonists but without inducing drug-seeking behavior, tolerance, or impaired motor and thermal regulation.This structure-based approach provides a blueprint for developing next-generation GPCR therapeutics with dissociated signaling profiles, offering a promising alternative to opioid-based pain management.
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  • Gao Zhihua's group published in Neuron
    27 02
    A research article, entitled “More than microglial depletion: PLX5622 activates the hepatic constitutive androstane receptor to alter anesthesia and addiction” was published online in Neuron. This study was led by Prof. Zhihua Gao’s group at Zhejiang University School of Brain Science and Brain MedicineThis study provides the first evidence that PLX5622, a widely used CSF1R inhibitor for depleting microglia, has effects that extend beyond the central nervous system. In addition to inhibiting CSF1R in the brain, PLX5622 directly activates CAR (Constitutive Androstane Receptor), a hepatic xenobiotic sensor. This activation markedly enhances the metabolism of anesthetics and addictive substances, leading to significant changes in anesthetic sensitivity and addiction-related behaviors. These findings suggest that conclusions about microglial function drawn solely from experiments using PLX5622 may need to be carefully interpreted.Microglia, the brain’s resident immune cells, are essential for maintaining homeostasis and regulating neural function, including the modulation of neuronal activity, synaptic plasticity, and the pathology of neurological and psychiatric disorders. Pharmacologically depleting microglia by inhibiting CSF1R has become a key strategy for studying their roles and exploring therapies for neurodegenerative diseases. Among available inhibitors, PLX5622 is particularly popular due to its high specificity, oral bioavailability, and ability to cross the blood–brain barrier. Studies using PLX5622 have uncovered a range of unexpected microglial functions, which have generally been attributed to specific CSF1R inhibition and subsequent microglial loss. However, the potential off-target effects of this compound have not been systematically examined.This study reveals a previously unrecognized "central–peripheral" dual action of PLX5622: while it inhibits CSF1R in the central nervous system, it also activates a CAR-dependent xenobiotic metabolic program in the liver. This discovery has important implications for interpreting the results of the numerous studies that have relied on PLX5622 to investigate microglial function.Website: https://www.cell.com/neuron/fulltext/S0896-6273(25)01001-3
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  • HU Hailan’s group published in Neuron on the sexually dimorphic winner effect in mice
    27 10
    The research team led by Prof. Hailan Hu has recently published an article titled Neural mechanism of the sexually dimorphic winner effect in mice on Neuron online on Oct. 15, 2025. This research revealeddmPFC PV-INs as a target for enhancing the winner effect, establishing a circuit-level framework for sex differences in competitive behaviors.The ‘‘winner effect,’’ where prior victories increase the likelihood of future wins, profoundly shapes social hierarchy dynamics and competitive motivation. Although human literature suggests a less pronounced winner effect in females, the neural mechanisms underlying these sex differences remain unclear. Here, we show that, compared with male mice, female mice take longer to form social hierarchies and exhibit a weaker winner effect. The dorsomedial prefrontal cortex (dmPFC), crucial for social dominance in males, plays a similar role in female mice. However, female mice exhibit reduced long-term potentiation (LTP) at the mediodorsal thalamus (MDT)-to-dmPFC synapses. In vitro recordings revealed that female mice have heightened excitability of dmPFC parvalbumin interneurons (PV-INs). Modulation experiments revealed that PV-IN activity controls LTP at MDT-to-dmPFC synapses and dominance behavior in a sex-dependent manner: increasing PV-IN excitability in male mice suppressed LTP and weakened the winner effect, whereas reducing PV-IN excitability in female mice enhanced LTP and promoted the winner effect. These findings point to a model in which elevated GABAergic inhibition from dmPFC local PV-INs raises the threshold for LTP induction in females, dampening the winner effect. This work identifies dmPFC PV-INs as a target for enhancing the winner effect, establishing a circuit-level framework for sex differences in competitive behaviors.Sexually dimorphic winner effect driven by dmPFC PV interneuron excitabilityhttps://www.cell.com/neuron/fulltext/S0896-6273(25)00717-2HAILAN HU'S RESEARCH GROUP: For social animals, emotions and health are regulated by various social behaviors. Hailan Hu's group is dedicated to studying the neural basis and plasticity mechanisms of emotion and social behavior. They use cutting-edge techniques including imaging, electrophysiology (both in vitro and in vivo), molecular genetics, and optogenetics to conduct deep analysis of emotion- and social behaviors- and their related neural circuits.
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  • GONG Zhefeng's group Publishes in Physical Review Letters on Muscle Mechanics of Drosophila Larva Rolling Motion
    16 06
     The research team led by Prof. Zhefeng Gong has recently published an article titled "Mechanics of Soft-Body Rolling Motion Without External Torque" in Physical Review Letters on May 16th, 2025. This study reveals the muscle-driven mechanism behind the torque-free rolling motion of Drosophila larvae and validates the findings through a bio-inspired soft robot.   Muscle activation sequence enables self-driven rolling without external torque.   While rolling motion is challenging for most animals (e.g., spiders relying on gravity or caterpillars using abrupt bending), Drosophila larvae can perform continuous, rapid rolling to escape predators. Conventional theories suggested this motion required external torque from gravity or ground reaction forces, but experimental data showed larvae generate tangential forces far exceeding gravity and can even roll upside down.   Through transgenic muscle labelling and light-sheet microscopy, the team discovered that axial muscles alternately contract and relax when larvae bend into a C-shape, creating sequential torque for continuous rolling. Precise ablation experiments confirmed axial muscles' essential role—their removal stopped rolling completely, while circumferential muscle ablation only reduced speed.   The team developed a biomechanical model treating the larva as a fluid-filled elastic cylinder. The model demonstrates: Higher internal pressure enables greater body curvature, enhancing rolling efficiency. Segmented axial muscles generate additive torque. Rolling direction is determined by muscle activation sequence, not C-shape orientation. Motion follows angular momentum conservation in absence of external torque. To validate the model, researchers built a pneumatic soft robot with four inflatable chambers mimicking muscle activation. Despite using elongation (rather than contraction) for actuation, the robot achieved continuous rolling with larval-like robustness, even compensating for failed chambers. This work not advances understanding of neural circuits controlling soft-body locomotion but also provides design principles for bio-inspired robots. The torque-free mechanism could enable future robots to navigate complex environments without relying on external forces.   The muscle contraction sequence of the rolling behaviour in larvae and its mechanical modelWebsite: https://journals.aps.org/prl/abstract/10.1103/PhysRevLett.134.198401ZHEFENG GONG'S RESEARCH GROUP: The team studies neural control mechanisms of soft-body movement using Drosophila larvae as a model organism, with applications in bionics and robotics. Their work has been published in Science, Nature Communications, Current Biology, and Physical Review Letters.  
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  • YANG Hongbin's group published in Nature Communications on negative valence coding by noise
    19 05
    The research team led by Dr. Hongbin Yang has recently published an article titled “A midbrain circuit mechanism for noise-induced negative valence coding” on May 17, 2025. This study revealed how noise affects emotional behaviors through a non-classical auditory pathway.Unpleasant sounds can elicit a range of negative emotional reactions and even pain. The neural pathways that transform auditory stimuli into salient actions have been extensively studied, the neural mechanisms that convert sounds into emotions remain unclear. In this study, the researchers discovered that glutamatergic neurons in the central inferior colliculus (CICglu) relay noise information to GABAergic neurons in the ventral tegmental area (VTAGABA) via the cuneiform nucleus (CnF), thereby encoding negative emotions in mice. In contrast, the canonical auditory pathway from the central inferior colliculus to the medial geniculate nucleus (CICglu→MG) is responsible for processing salient stimuli. By combining viral tracing, calcium imaging, and optrode recording, they demonstrated that the CnF acts downstream of CICglu to convey negative valence to the mesolimbic dopamine system by activating VTAGABA neurons. Optogenetic or chemogenetic inhibition of any connection within the CICglu→CnFglu → VTAGABA circuit, or direct excitation of the mesolimbic dopamine (DA) system, is sufficient to alleviate noise-induced negative emotion perception. Website: https://www.nature.com/articles/s41467-025-59956-zMotivated behavior arises through approaching a reward or avoiding punishment. These behaviors control an animal's interactions with those goal objects in the environment that are important for the survival of the individual and the species. Many mental diseases (for example, depression and addiction etc.) are associated with dysfunction of the neuronal circuits of motivated behaviors. Hongbin Yang's group is dedicated to studying the neural basis mechanisms of motivated behavior. They use cutting-edge techniques, including imaging, electrophysiology (both in vitro and in vivo), molecular genetics, and optogenetics to understand how sensory inputs, arousal states, and motor systems make up the motivated behaviors.  
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  • HU Hailan's group published in Cell on Neuron-astrocyte Coupling
    25 04
    The research team led by Professor Hailan Hu has recently published a groundbreaking article titled Neuron-astrocyte Coupling in Lateral Habenula Mediates Depressive-like Behaviors in Cell on April 24th, 2025. This study reveals how brain cells dynamically cooperate to drive stress response and depression.Stress-induced depression-like behaviors are driven by a dynamic recurrent network involving neurons and astrocytes in the lateral habenula and norepinephrine release from neurons in the locus coeruleus in freely-moving mice.The lateral habenular (LHb) neurons and astrocytes have been strongly implicated in depression etiology but it was not clear how the two dynamically interact during depression onset. Here, using multi-brain-region calcium photometry recording in freely-moving mice, we discover that stress induces a most rapid astrocytic calcium rise and a unique bimodal neuronal response in the LHb. LHb astrocytic calcium requires the α1A-adrenergic receptor, and depends on a recurrent neural network between the LHb and locus coeruleus (LC). Through the gliotransmitter glutamate and ATP/Adenosine, LHb astrocytes mediate the second-wave LHb neuronal activation and norepinephrine (NE) release. Activation or inhibition of LHb astrocytic calcium signaling facilitates or prevents stress-induced depressive-like behaviors respectively. These results identify a stress-induced positive feedback loop in the LHb-LC axis, with astrocytes being a critical signaling relay. The identification of this prominent neuron-glia interaction may shed light on stress management and depression prevention.LHb neuron-astrocyte synergy in depressionWebsite: https://doi.org/10.1016/j.cell.2025.04.010
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    • Speaker：Georg Northoff

      Institution：University of Ottawa

      Time：28th May，14:30AM

      Locatiom：Zhonglan Meeting Room

      Intrinsic Neural Timescales - Spatiotempora lApproach to Conscious...

    • Speaker： Li Zhang

      Institution：University of Southern California

      Time：26th May, 9:30AM

      Locatiom：Meeting Room 705

      Neural Circuitry for Motivated Behaviors

    • Speaker： Cory T. Miller

      Institution：University of California San Diego

      Time：23th April, 10:00 Am

      Locatiom：Room 205, School of Medicine

      Resolving the Cocktail Party Problem

    • Speaker：Chen Tao

      Institution：Air Force Medical University of PLA

      Time：11th December，10:00 AM

      Locatiom：Meeting Room 705

      Opposing regulation of affective versus physical pain in the insul...

    • Speaker：Julio Licino

      Institution：Medical University

      Time： 14th October，15:00 PM

      Locatiom： Liangzhu Laboratory

      PHF21B and the Epigenetic Mechanisms Underlying Social Memory Form...

    • Speaker：WANG Yutian

      Institution：Fudan University

      Time：13th October，10:00 AM

      Locatiom：Liangzhu Laboratory

      Mechanisms underlying synaptic plasticity and their roles in lear...

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        School of Brain Science and Brain Medicine Zhejiang University

        The School of Brain Science and Brain Medicine, devoted to the study of neuroscience and neuromedicine, was founded in October 2019. As the first school focusing on brain science and brain medicine in Chin... 【More】

        Address : Zijingang Campus of Zhejiang University

        Tel : 0571-87071107

        E-mail : brains@zju.edu.cn

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