NEWS

Hongbin Yang’s group published in Nature Communications on negative valence coding by noise

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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Hailan Hu's group published in Cell on Neuron-astrocyte Coupling

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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Jiadong Chen' group published in Journal of Clinical Investigation on molecular markers of neuronal senescence in human drug-resistant epilepsy

Epilepsy is a chronic neurological disorder caused by abnormal discharges of neurons in the brain and is often accompanied by symptoms such as cognitive impairment, anxiety, depression, and autism, severely affecting patients' quality of life. Globally, approximately 70 million people suffer from epilepsy, with an incidence rate of about 6.4 per 1,000 people. Among them, around 30% do not respond to existing antiepileptic drugs and are classified as "drug-resistant epilepsy," though its exact pathogenesis remains unclear. Studies have shown distinct pathological characteristics from the epileptic focus of brain tissue of patients with drug-resistant epilepsy. For example, patients with focal cortical dysplasia (FCD) epilepsy have dysmorphic neurons in the gray matter and balloon cells in the white matter, whereas patients with temporal lobe epilepsy (TLE) display neuronal loss and hippocampal sclerosis. Understanding the gene expression characteristics of these pathological neuronal cells is crucial for investigating the diagnosis and pathogenesis of drug-resistant epilepsy.Dr. Jiadong Chen’s group at Zhejiang University published an article online in the Journal of Clinical Investigation titled “Multimodal single-cell analyses reveal molecular markers of neuronal senescence in human drug-resistant epilepsy”on March 3, 2025. The study utilized Patch-seq, a technique combining patch-clamp electrophysiology with single-cell sequencing, to precisely analyze the electrophysiological properties, morphology, and gene expression of pathological neurons in drug-resistant epilepsy. We identified a unique subpopulation of cortical pyramidal neurons that highly express genes associated with the mTOR pathway, inflammatory responses, and cellular senescence, such as CDKN1A (P21)、CCL2 and NFKBIA. Furthermore, pathological neurons in the brain tissue of drug-resistant epilepsy patients exhibited increased expression of senescence markers (P21、P53、COX2、γ-H2AX、β-Gal）and a reduction in the nuclear integrity marker Lamin B1. These changes were observed in the brain tissue of drug-resistant epilepsy across different pathologies, but were absent in control brain tissues from individuals without epilepsy. Additionally, in a mouse model of drug-resistant epilepsy, we found that chronic seizures—rather than acute seizures—induced the expression of cortical neuronal senescence markers, further supporting the role of neuronal senescence in epilepsy pathogenesis. Professor Gemma L. Carvill from Northwestern University positively acknowledged our work in JCI: "Neuronal senescence is prevalent in aging as well as in neurodegenerative disease. However, a role for senescence in epilepsy is virtually unexplored. In this issue of the JCI, Ge and authors used resected brain tissue from individuals with drug-resistant epilepsy, a genetic knockout mouse model, and a chemoconvulsant mouse model, to demonstrate a subset of cortical pyramidal senescent neurons that likely contribute to the pathophysiology of epilepsy. These findings highlight senescence as a possible target in precision-therapy approaches for epilepsy and warrant further investigation." Figure 1. Patch-seq reveals the morphological, electrophysiological and molecular markers of pathological neurons in drug-resistant epilepsyThis study was jointly conducted by Ph.D. students Qianqian Ge, Jiachao Yang (currently a postdoctoral researcher at the Department of Brain Science and Brain Medicine, Zhejiang University), Fei Huang, Xinyue Dai, and Chao Chen, in collaboration with Professor Li Shen’s laboratory at Zhejiang University and Professor Shengjin Xu’s laboratory at the Institute of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences. The study also received valuable support from the teams of Professors Shumin Duan, Xiaoming Li, Jianmin Zhang, and Junming Zhu at Zhejiang University, as well as the National Health and Disease Human Brain Tissue Resource Bank.The Jiadong Chen's group at Zhejiang University School of Medicine is dedicated to functional genomics research in neuroscience by integrating single-cell genomics, calcium imaging, and electrophysiology. Recent research findings have been published in international journals including Journal of Clinical Investigation (2025), Nature Communications (2025, accepted), Advanced Science (2024), and Neuroscience Bulletin (2022, 2023). Our lab is currently recruiting postdoctoral researchers interested in neurobiology, cell biology, and genomics, offering competitive benefits. Interested candidates are invited to send their CV and research interests to jardongchen@zju.edu.cn.Related paper：https://www.jci.org/articles/view/188942 (doi: 10.1172/JCI188942)Comment by Professor Gemma L. Carvill: https://www.jci.org/articles/view/189519

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Lijun Kang's group published in Nature Communications on mechanosensation

Mechanotransduction plays a critical role in various physiological processes, including hearing, touch, proprioception, pain, and blood pressure regulation. Mechanogated ion channels function as mechanoreceptors, converting mechanical forces into electrical signals to transduce force information. To date, all known mechanotransduction channels in the animal kingdom are either cation channels or channels permeable to cations (such as Piezo1/2, TMC1, TRP-4/NomPC/TRPN, ENaC, TMEM63, and K2P), with no reports of anion channels.On February 16, 2025, Professor Lijun Kang’s team from the School of Brain Science and Brain Medicine, Zhejiang University School of Medicine, published a research article entitled “Anoctamin-1 is a core component of a mechanosensory anion channel complex in C. elegans” in Nature Communications. In this study, they discovered that the calcium-activated chloride channel Anoctamin-1 (ANOH-1) mediates touch sensation of male C. elegans by directly sensing mechanical forces. The human homolog ANO1/TMEM16A shares similar mechanosensitive properties. Furthermore, mechanotransduction via ANOH-1/ANO1 requires the involvement of auxiliary molecules CIB2 and Ankrin. In previous studies, Professor Lijun Kang’s team identified the multimodal functions of the Beethoven gene tmc1 and clarified its mechanism, proposing a dual-tether model of TMC1 as the mechanotransductive cation channel in hearing (Neuron 2018, 2021, 2024). In the current study, using molecular genetics, in vivo calcium imaging, patch-clamp electrophysiology, pharmacology, and behavioral analysis, they found that the calcium-activated chloride channel ANOH-1 is involved in the tactile responses of male C. elegans. Pharmacological and electrophysiological recordings indicated that ANOH-1 directly mediates mechanoreceptor currents (MRCs), and its mammalian homolog, ANO1, exhibits similar functions. Through gene screening and co-immunoprecipitation (Co-IP) experiments, they further found that mechanosensation by ANO1/ANOH-1 requires auxiliary molecules CIB2 and Ankrin. Interestingly, CIB2 and Ankrin are also necessary auxiliary molecules for the mechanotransduction of the TMC1 cation channel in the inner ear hair cells (Figure 1). This study, along with the team's previous research, reveals the molecular mechanisms underlying mechanotransduction in hearing, touch, and other modalities, laying the scientific foundation for research and drug development related to sensory disorders.Figure 1 Schematic of the TMC1 and ANO1 Mechanosensitive Complex. (Adapted from Neuron 2021, Neuron 2024, and Nature Communications 2025, published by Prof. Lijun Kang's group)---------------------------LIJUN KANG’S RESEARCH GROUPEmploying an interdisciplinary strategy that integrates molecular genetics, optogenetics, calcium imaging, electrophysiology, and behavioral tracking, research carried out in the Kang laboratory is dedicated to unravel the complex molecular mechanisms governing sensory perception, including olfaction, hearing, and tactile sensation. Utilizing C. elegans and various other model organisms, the laboratory delves into the physiological roles and mechanisms of glia in regulating sensory circuits. The laboratory also seeks to investigate pharmaceutical approaches for mitigating sensory dysfunctions stemming from genetic anomalies, aging, and other influential factors.

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MA Huan's group published in Science on mechanisms underlying dynamic brain energy supply

Prof. MA Huan's team at Zhejiang University investigated the relationship between neuroplastic regulation of bioenergetics and cognitive aging. Their findings, published in Science under the title Boosting neuronal activity-driven mitochondrial DNA transcription improves cognition in aged mice, provide a novel perspective and theoretical framework for understanding energy-efficient neural computation and combating cognitive aging.As the core organ governing thought and consciousness, the brain consumes immense biological energy to maintain critical functions such as learning, memory, and emotions. To enable energy-efficient operation, the brain must finely regulate this process, achieving massive parallel information processing and storage at low energy costs. This high-efficiency, low-energy capability remains the ultimate goal of supercomputing and AI technologies, yet it is a peak still beyond human technological reach. Moreover, energy regulation in the brain is closely tied to human health, as its imbalance is considered a major risk factor for neurological disorders, particularly age-related neurodegenerative diseases.Whether it is the energy crisis posed by AI's high energy consumption or the challenges of cognitive decline in aging populations, these are critical issues for humanity. From a scientific perspective, understanding how mammalian brains integrate energy, matter, and information—the fundamental elements of universe offers not only pathways to mimic and surpass the brain's evolved low-energy, high-efficiency mechanisms but also opportunities to address age-related challenges. Driving mitochondrial gene transcription with mental activityThe brain's hallmark is its ability to dynamically adjust the strength of neuronal connections based on activity and experience—termed synaptic plasticity. This plasticity relies on activity-driven transcription of nuclear genes, producing new proteins essential for learning and memory. Mitochondria, as the primary energy providers, are unique organelles with their own genome, and mitochondrial transcription is crucial for energy supply and biogenesis. The central question is: Can neuronal activity regulate mitochondrial gene transcription (E-TCmito), similar to its regulation of nuclear transcription? If so, this coupling would enable coordinated transformation of energy and matter to support information transmission and storage. Using mouse models, Prof. Ma's team discovered that enhanced neuronal activity—whether during learning or artificially induced—significantly increased mitochondrial gene transcription near synapses. Further investigation revealed that this activity-mitochondrial transcription coupling depends heavily on mitochondrial calcium influx induced by neuronal activity. This process is regulated by mitochondrial CaMKII (CaMKIImito). Once mitochondrial calcium levels rise, calcium-responsive transcription factor CREBmito binds to the D-loop region of the mitochondrial genome, driving gene transcription. Notably, both CaMKII and CREB are traditionally considered key regulators of nuclear gene transcription, and their newfound role in mitochondria challenges textbook definitions, showcasing their multifaceted functions in the nervous system. By dissecting these mechanisms, the team achieved precise molecular control over activity-driven mitochondrial transcription. They demonstrated that this process is essential for mitochondrial biogenesis, quality control, and the dynamic regulation of energy during neuronal activity—providing a foundation for maintaining synaptic function and cognitive processes such as learning and memory. Can mental exercises rejuvenate the aging brain?Research has shown that brain energy supply and cognitive ability decline with aging or neurodegeneration. The team observed that activity-driven mitochondrial transcription coupling weakens in aged brains. We speculated whether enhancing this coupling could improve brain function and counteract cognitive aging, said Dr. LI Wenwen. Using transgenic mouse models, they confirmed that suppression of this coupling led to energy deficits and cognitive impairments similar to aging-related neuropathology. To address this, the team developed molecular tools to precisely enhance neuronal activity-mitochondrial transcription coupling. Experiments revealed that prolonged enhancement of this mechanism boosted mitochondrial gene expression during learning, increased energy supply, and significantly improved cognitive performance in aged mice. This provides theoretical evidence that mental exercises can counteract brain aging, Dr. Li added. Unraveling this fundamental signaling mechanism in neurons not only deepens understanding of brain function but also offers a new molecular framework for combating cognitive decline. Ongoing translational research and drug development have shown encouraging results.Implications for Energy-Efficient Artificial IntelligenceElon Musk has highlighted that, beyond chip shortages, energy will be the next bottleneck for AI computation. Could the brain's low-energy information processing inspire solutions to AI's energy demands? Prof. Ma's team recognized that the evolutionary mechanism of neuronal activity-mitochondrial transcription coupling might hold the key. Unlike traditional computers, which rely on uniform energy supply, the mammalian brain employs a unique on-demand energy strategy: mitochondria near synapses act as energy packets regulated by local neuronal activity. This discovery suggests that the brain achieves efficient, low-energy computation by dynamically regulating local energy production at each data node (synapse). “Revealing this fundamental coupling mechanism may help AI systems enhance computational efficiency while reducing energy consumption,” said Prof. Ma.Related paper:Li, W., Li, J., Li, J., Wei, C., Laviv, T., Dong, M., Lin, J., Calubag, M., Colgan, L., Jin, K., et al., (2024). Boosting neuronal activity-driven mitochondrial DNA transcription improves cognition in aged mice. Science 386, eadp6547.Lab Introduction:In Ma lab, we are passionate about studying the brain, embracing youth and dreams, and cherishing moments with friends to recall the past and imagine the future! Guided by clinical data and using transgenic mouse models, our lab employs electrophysiology, molecular biology, and behavioral analysis to conduct both fundamental and translational research. Our main research focuses include neuroplasticity, learning and memory, aging, and sex dimorphism. Our findings have been published in prestigious journals such as Science, Cell, and Neuron.Contact of the lab: mah@zju.edu.cnSource: The research team led by Prof. MA Huan

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Hailan Hu's group published in Neuron on neural mechanism underlying social hierarchy

The research team led by Prof. Hailan Hu has recently published an article titled Deconstructing the neural circuit underlying social hierarchy in mice on Neuron online on Dec 10th, 2024. This research revealed the antagonistic interplay between win-related and lose-related dmPFC downstream pathways in mediating social competition.Social competition determines hierarchical social status, which profoundly influences animals’ behavior and health. The dorsomedial prefrontal cortex (dmPFC) plays a fundamental role in regulating social competitions, but it was unclear how the dmPFC orchestrates win- and lose-related behaviors through its downstream neural circuits. Here, we dissected the individual contribution and reciprocal interaction of dmPFC downstream circuits in modulating dominance behavior. Brain-wide c-Fos mapping experiment revealed that winner mice in the tube test competition exhibited a significantly higher number of c-Fos-positive neurons in the dmPFC downstream targets, including the DRN and PAG, whereas loser mice exhibited more c-Fos-positive neurons in the aBLA. Consistently, pathway-specific manipulations outlined a dmPFC-centric social dominance neural network, in which the dmPFC-DRN and dmPFC-PAG circuits act as win-related pathways, whereas the dmPFC-aBLA circuit acts as a lose-related pathway. Moreover, the activation or inhibition of the aBLA itself yielded similar effects as manipulation of the dmPFC-aBLA pathway. Accordingly, these win- and lose-related dmPFC circuits showed opposing calcium activities when mice initiated ‘‘effortful’’ push behaviors in the tube test competition. Retrograde tracing study revealed that these functionally divergent pathways are anatomically segregated, with the lose-related aBLA-projecting neurons located in the layer 2/3 and the win-related DRN- and PAG- projecting neurons located in the layer 5 of the dmPFC. Finally, using in vivo and in vitro electrophysiological recordings, we found an inhibition from the lose-related neurons to the win-related neurons through local PV and SST interneurons in the dmPFC. One interesting speculation of the function of this unidirectional interaction is that losing mentality may dominate over winning during competitions: once animals initiate the idea of quitting or withdrawing from the rivalry, the inhibition on the win pathway from the lose pathway would help them execute the idea and end the fight quickly. Such antagonistic interplay may represent a central principle in how the mPFC orchestrates complex behaviors through top-down control.dmPFC-centric social dominance neural networkhttps://www.cell.com/neuron/abstract/S0896-6273(24)00807-9HAILAN 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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Shumin Duan and Yan-qin Yu 's group published in Advanced Science on astrocytes and arousal

The research team led by Prof. Shumin Duan and Yan-qin Yu has recently published a study in Advanced Science titled Adenosine‐Dependent Arousal Induced by Astrocytes in a Brainstem Circuit on October 16, 2024 This study provides the first evidence that astrocytes in the brainstem parafacial zone (PZ) play a unique role in promoting and sustaining wakefulness through extracellular adenosine and elucidates the underlying circuit-level mechanisms.Astrocytes play a crucial role in regulating sleep-wake behavior. However, how astrocytes govern a specific sleep-arousal circuit remains unknown. Here, the authors show that parafacial zone (PZ) astrocytes responded to sleep-wake cycles with state-differential Ca2+ activity, peaking during transitions from sleep to wakefulness. Using chemogenetic and optogenetic approaches, they found that activating PZ astrocytes elicited and sustained wakefulness by prolonging arousal episodes, while impeding transitions from wakefulness to non-rapid eye movement (NREM) sleep. Activation of PZ astrocytes specially induced the elevation of extracellular adenosine through the ATP hydrolysis pathway but not equilibrative nucleoside transporter (ENT) mediated transportation. Strikingly, the rise in adenosine levels induced arousal by activating A1 receptors, suggesting a distinct role for adenosine in the PZ beyond its conventional sleep homeostasis modulation observed in the basal forebrain and cortex. Moreover, at the circuit level, PZ astrocyte activation induced arousal by suppressing the GABA release from the PZGABA neurons, which promote NREM sleep and project to the parabrachial nucleus (PB). Thus, their study unveils a distinctive arousal-promoting effect of astrocytes within the PZ through extracellular adenosine, and elucidates the underlying mechanism at the neural circuit level. Summary of the molecular and neural circuit mechanisms underlying PZ astrocyte activation in sleep-wake regulation.Website: https://onlinelibrary.wiley.com/doi/10.1002/advs.202407706SHUMIN DUAN AND YAN-QIN YU'S RESEARCH GROUP: Shumin Duan and Yan-qin Yu's group is dedicated to studying the roles of glial cells in synaptic plasticity and the mechanisms of neuron-glia interactions in health and disease. They use cutting-edge techniques including imaging, fiber photometry, electrophysiology (both in vitro and in vivo), molecular genetics, and optogenetics to conduct deep analysis of higher brain functions such as sensory processing, sleep-wake modulation, and emotion-related diseases such as anxiety and depression, learning and memory.

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Xiao-Ming Li and Jiadong Chen 's group published in Advanced Science on the neural mechanism of amygdala in regulating temporal lobe epilepsy

The research team led by Prof. Xiao-Ming Li and Jiadong Chen has recently published an article titled Posterior Basolateral Amygdala is a Critical Amygdaloid Area for Temporal Lobe Epilepsy in Advanced Science on October 30, 2024. This research revealed the pBLA as a pivotal nucleus in the amygdaloid complex for regulating epileptic seizures in TLE.The amygdaloid complex consists of multiple nuclei and is a key node in controlling temporal lobe epilepsy (TLE) in both human and animal model studies. However, the specific nucleus in the amygdaloid complex and the neural circuitry governing seizures remain unknown. Here, it is discovered that activation of glutamatergic neurons in the posterior basolateral amygdala (pBLA) induces severe seizures and even mortality. The pBLA glutamatergic neurons project collateral connections to multiple brain regions, including the insular cortex (IC), bed nucleus of the stria terminalis (BNST), and central amygdala (CeA). Stimulation of pBLA-targeted IC neurons triggers seizures, whereas ablation of IC neurons suppresses seizures induced by activating pBLA glutamatergic neurons. GABAergic neurons in the BNST and CeA establish feedback inhibition on pBLA glutamatergic neurons. Deleting GABAergic neurons in the BNST or CeA leads to sporadic seizures, highlighting their role in balancing pBLA activity. Furthermore, pBLA neurons receive glutamatergic inputs from the ventral hippocampal CA1 (vCA1). Ablation of pBLA glutamatergic neurons mitigates both acute and chronic seizures in the intrahippocampal kainic acid-induced mouse model of TLE. Together, these findings identify the pBLA as a pivotal nucleus in the amygdaloid complex and offer novel circuit mechanisms of pBLA in regulating epileptic seizures in TLE. This insight holds promise for advancing more precise, circuit-targeted therapies for TLE. Model diagram showing the role of pBLA glutamatergic neurons and their collateral projections in epileptic seizures in TLE Website: https://doi.org/10.1002/advs.202407525 Xiao-Ming Li's RESEARCH GROUP: Dr Xiao-Ming Li's group is focusing on the research of different synapses and neural circuits, seeking treatment for mental illnesses such as anxiety, depression and schizophrenia by revealing approachable molecular targets and designing corresponding treatment strategies. The main research content is:1) Research on the neural circuit of emotional and affective disorders2) Pathogenesis study of neuropsychiatric diseases such as anxiety, depression and schizophrenia3) Basic and clinical research on neuropsychiatric diseases such as anxiety, depression and schizophrenia (Clinical)

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SEMINARS

Speaker：Dick F. Swaab

Institution：Royal Netherlands Academy of Arts and Sciences

Time：13th May, 2PM

Locatiom：Fulou Meeting Room

The Neurobiology of stress, Depression and Suicide

Speaker：Guoqiang Yu

Institution：Tsinghua University

Time：9th April, 10AM

Locatiom：Liangzhu Laboratory

Quantification and Analysis of Molecular Spatiotemporal Signals wi...

Speaker：JACK L. FELDMAN

Institution：University of California Los Angeles

Time：7th April, 10AM

Locatiom：Liangzhu Laboratory

Breathing Matters

Speaker：Erquan Zhang

Institution：National Institute of Biological Sciences

Time：7th April, 3:30PM

Locatiom：Liangzhu Laboratory

Towards A Grand Unified Theory for the Circadian Clock

Speaker：Yang Zhan

Institution：Shenzhen Institute of Advanced Technology，Chinese

Time：March 6th, 10AM

Locatiom：Meeting Room 705

Coding patterns in the prefrontal-subcortical circuit during soci...

Speaker：Ji Hu

Institution：ShanghaiTech University

Time：March 5th, 10AM

Locatiom：Liangzhu Laboratory

Reverse-translational study of neuropharmacology and neuropsychiat...

NEWS

SEMINARS

The Neurobiology of stress, Depression and Suicide

Quantification and Analysis of Molecular Spatiotemporal Signals wi...

Breathing Matters

Towards A Grand Unified Theory for the Circadian Clock

Coding patterns in the prefrontal-subcortical circuit during soci...

Reverse-translational study of neuropharmacology and neuropsychiat...

FACULTY

School of Brain Science and Brain Medicine Zhejiang University