• 02 04
    Jianhong Luo lab from the School of Brain Science and Brain Medicine at Zhejiang University published a paper in Molecular Psychiatry, revealing the mechanisms of frontal-striatal circuit dysfunction that lead to cognitive inflexibility in the autism mouse model NL3R451C. Cognitive flexibility is an important component of executive function, enabling animals to respond appropriately to constantly changing environment. Autism Spectrum Disorder (ASD) is characterized by social deficit, repetitive, stereotyped behaviors and limited interests, the underlying mechanisms of which may involve deficits in cognitive/behavioral flexibility.Neuroligin-3 (NL3) is significant in synapse formation and function, and its R451C missense mutation is associated with ASD. The knock-in mouse model NL3R451C exhibits autistic-like characteristics. Using two alternative forced choice task, the authors found that NL3R451C mice exhibited behavioral inflexibility in dynamic learning tasks.To investigate the neural mechanism of decision-making flexibility in reward-based learning tasks, the authors conducted single-neuron firing rate analyses and discovered that medium spiny neurons (pMSN) in the nucleus accumbens (NAc) of knock-in (KI) mice showed enhanced response to cue stimuli, and the modulation of their firing rate changes by previous task outcomes was reduced, indicating impaired experience-dependent neural plasticity. Role of midbrain-limbic dopamine (DA) signaling in the cognitive rigidity of KI mice was then studied, it was observed that DA dynamics and reward prediction error (RPE) signals, which are used for motivation and guiding goal-directed learning, were significantly disrupted in KI mice, hindering the acquisition of new strategies in set-shifting tasks. Subsequently, authors found that the medial prefrontal cortex (mPFC)-NAc circuit in KI mice was impaired using fiber photometry recording. Re-expression of NL3 in the mPFC could effectively rescue the cognitive inflexibility phenotype of KI mice, while simultaneously reconstructing the output of the mPFC-NAc, NAc MSN encoding, and DA signal dynamics, establishing the crucial role of mPFC in the cognitive flexibility deficits of NL3R451C mice.In summary, this study reveals the association between frontal-striatal circuit functional and DA modulation dysfunction and cognitive inflexibility in ASD mice, providing new insights into the neural mechanisms of cognitive/behavioral flexibility deficits and offering potential new strategies for intervention. 
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  • 08 03
    Glial cells play a crucial role in the development, function, and health of the nervous system and brain. From Caenorhabditis elegans, Drosophila to zebrafish, mice, and humans, the origin, structure, and function of glial cells have been highly conserved [1].On March 6, 2024, Professor Lijun Kang and his team published a research article titled "Phasic/Tonic-like Glial GABA Differentially Transduce for Olfactory Adaptation and Neuronal Aging" in the journal Neuron. In their study, they discovered that AMsh glial cells regulate real-time olfactory adaptation and long-term neuronal aging through two distinct GABA signaling pathways (Figure 1) [2].Figure 1: Differential regulation of olfactory adaptation and neuronal aging by phasic/tonic-like glial GABA signaling.Adaptability is one of the fundamental characteristics of the nervous system. In their previous research, Professor Lijun Kang's team revealed that sheath-like glial cells called AMsh glia sense odorant stimuli via G-protein coupled receptors (GPCRs) in the chemosensory organ of C. elegans. These glial cells release GABA, which acts on the GABAA receptor LGC-38 in ASH sensory neurons, leading to the inhibition of their activity and promoting olfactory adaptation. This work proposed a dual receptor model involving glial cells and neurons for olfactory sensation, emphasizing the essential role of glial cells as driving forces behind neuronal adaptation (Neuron 2020) [3].In their recent publication in Neuron, Professor Lijun Kang's team demonstrated that AMsh glial cells elevate cytoplasmic calcium levels upon sensing odorant stimuli. This elevation triggers the secretion of GABA from vesicles, a process dependent on the vesicular GABA transporter UNC-47/VGAT. The released GABA acts on ASH sensory neurons to facilitate olfactory adaptation. Additionally, at resting calcium levels, AMsh glial cells can gradually release GABA through bestrophin ion channels (Best-9/-13/-14), which activates the GABAB receptor GBB-1 on ASH sensory neurons, and regulates the activity of the transcription factor HSF-1 via the PLCβ signaling pathway, thus slowing down the aging process of ASH neurons.This research has revealed two distinct GABA signaling pathways within the local circuitry involving AMsh glial cells and ASH sensory neurons. Each pathway plays crucial physiological roles: (1) UNC-47/VGAT--LGC-38/GABAA fast signaling pathway. The key gene UNC-47 is predominantly expressed in the soma and proximal processes of AMsh glial cells, while LGC-38 is localized to the soma and axons of ASH neurons. (2) Bestrophin channels--GBB-1/GABAB slow signaling pathway. The critical genes, the bestrophin channels and GBB-1, are extensively expressed in AMsh glial cells and ASH neurons, respectively. Notably, UNC-47/VGAT-dependent GABA release is triggered by high calcium levels, whereas bestrophin channels can release GABA under low calcium conditions. Furthermore, GBB-1/GABAB receptors exhibit higher affinity for GABA compared to LGC-38/GABAA receptors. These findings provide novel insights into the significant role of glial cells in sensory encoding and neuronal aging.References:(1) Nagai et al., Behaviorally consequential astrocytic regulation of neural circuits. Neuron (2021) 109, 576-596.(2) Cheng et al., Phasic/Tonic-like Glial GABA Differentially Transduce for Olfactory Adaptation and Neuronal Aging. Neuron. 2024 Mar 1:S0896-6273(24)00090-4. doi: 10.1016/j.neuron.2024.02.006.(3) Duan et al. Sensory glia detect repulsive odorant and drive olfactory adaptation. Neuron (2020) 108,707-721.
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  • 08 03
    The research team led by Prof. Yan-qin Yu has recently published an article titled Control of defensive behavior by the nucleus of Darkschewitsch GABAergic neurons in National Science Review on Mar 5th, Beijing time. This research identifies a previously unrecognized role for the lPAGglu-NDGABA-GiVglu pathway in controlling defensive behaviors.Threatening situations, such as the presence of a predator or exposure to stimuli predicting imminent or perceived danger, evoke an evolutionarily conserved brain state, fear, which triggers defensive behaviors to avoid or reduce potential harm.The defensive behaviors to threats play a fundamental role in survival. Several brain areas have been implicated in defensive behaviors, including periaqueductal gray, amygdala, hypothalamus. But many nuclei which play important roles in defensive behaviors remain to be discovered.The nucleus of Darkschewitsch (ND), mainly composed of GABAergic neurons, is recognized as a component of the eye-movement controlling system. However, the functional contribution of ND GABAergic neurons (NDGABA) in animal behavior is largely unknown. Here, we show that NDGABA neurons were selectively activated by different types of fear stimuli, such as predator odor and foot-shock. Optogenetic and chemogenetic manipulations revealed that NDGABA neurons mediate freezing behavior. Moreover, using circuit-based optogenetic and neuroanatomical tracing methods, we identified an excitatory pathway from the lateral periaqueductal grey (lPAG) to the ND that induces freezing by exciting ND inhibitory outputs to the motor-related gigantocellular reticular nucleus, ventral part (GiV). Together, these findings indicate the NDGABA population as a novel hub for controlling defensive response by relaying fearful information from lPAG to GiV, a mechanism critical for understanding how the freezing behavior is encoded in the mammalian brain. Our results advance the current understanding of how threats selectively trigger freezing, a specific defensive response, via the lPAGGlu-NDGABA-GiVGlu circuitry and provide precise anatomical and functional information that is important for the discovery and development of new therapeutic interventions for mood disorders.Prof. Yan-qin Yu from Zhejiang University School of Medicine is the main corresponding author. Prof. Hongbin Yang from Zhejiang University MOE Frontier Science Center for Brain Science & Brain-Machine Integration is co-corresponding author. This research was strongly supported by Prof. Shumin Duan from Zhejiang University School of Medicine. Dr. Huiying Zhao, Jinrong Liu and Yujin Shao are the first authors. This work was mainly supported by STI2030-Major Projects and the National Natural Science Foundation of China.
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  • 14 02
    Excessive or repetitive fear play a significant role in the development of anxiety disorders, with the amygdala serving as the central locus for fear processing. Clinical research has demonstrated that individuals with bilateral amygdala damage are still capable of experiencing fear, indicating the amygdala may not be absolutely required for fear. To date, the neural mechanisms underlying fear that are independent of the amygdala are still poorly understood.On February 12th, Prof. LI Xiao-Ming and his team from the Zhejiang University School of Medicine published an article entitled A molecularly defined amygdala-independent tetra-synaptic forebrain-to-hindbrain pathway for odor-driven innate fear and anxiety on Nature Neuroscience. The study revealed the significant role of the main olfactory bulb → dorsal peduncular cortex → lateral parabrachial nucleus → parasubthalamic nucleus pathway in fear and anxiety (Figure 1).Figure 1 The schematic diagram of the main olfactory bulb → dorsal peduncular cortex → lateral parabrachial nucleus → parasubthalamic nucleus pathway Olfaction serves as a common sensory modality that elicits innate fear in animals. Through the use of 2,4,5-trimethyl-3-thiazoline (TMT), a compound present in fox feces, which is a stimulus with fear-eliciting properties for rodents, the research team observed a notable decrease in aversive and freezing behaviors triggered by TMT in mice, accompanied by the apoptosis of neurons in the cortical amygdala and medial amygdala. However, this kind of apoptosis did not have a significant impact on TMT-induced escape behavior. Therefore the team focused on finding the specific brain region that mediate the olfaction-evoked escape behavior.In the subsequent experiments, Dr. WANG Hao, the first author of the study, characterized neuronal activity as reflected in Fos expression in response to TMT. He observed a notable elevation in Fos expression in the dorsal peduncular cortex (DP), which receives distinct inputs from the main olfactory bulb (MOB). In addition, the MOB-DP neural circuit exhibits markedly heightened activity following TMT stimulation (Figure 2).Figure 2The MOB-DP neural circuit is involved in TMT-induced innate fear."The role of DP in olfaction-evoked innate fear was investigated by inhibiting DP neurons in mice using an apoptosis virus, which resulted in the absence of obvious escape behavior in response to TMT stimulation and a significant reduction in aversive and freezing behaviors. Conversely, activating DP neurons using optogenetics induced escape behavior in mice, along with observable fear-like reactions such as dilated pupils and decreased heart rate," explained Dr. WANG Hao.Concurrently, the team integrated optogenetic inhibition of DP neuron function with localized amygdala damage in mice. They observed that the combination of localized amygdala damage and DP inhibition resulted in a significant reduction of escape behavior induced by TMT in mice, as well as a further decrease in aversive and freezing behaviors. "Notably, the mitral/tufted cells projecting to DP and the cortical amygdala are two distinct groups of neurons. The aforementioned functional and structural observations suggest that DP is capable of autonomously mediating olfaction-evoked innate fear bypasses the amygdala,” stated Dr. WANG Qinng, co-first author of the study. Consequently, following input from the main olfactory bulb, how does the DP convey the fear response elicited by predator odor?Combining virus tracing and patch-clamp electrophysiology, the team have discovered that DP forms excitatory synaptic connections with cholecystokinin (Cck) positive neurons in the superficial lateral parabrachial nucleus (PBNsl), which then project to tachykinin 1 (Tac1) positive neurons in the parasubthalamic nucleus (PSTh). This results in the formation of a molecularly defined tetra-synaptic pathway: MOBSlc17a7+ → DPCamk2a+ → anterior PBNslCck+ → PSThTac1+.In order to investigate whether the tetra-synaptic pathway participate in olfaction-evoked innate fear, PhD candidates CUI Liuzhe  and FENG Xiaoyang delved deeper into the functional properties of the neural circuit. Their investigations revealed that this neural circuit exhibits significant activation during TMT-induced escape behavior (Figure 3). Furthermore, optogenetic inhibition of this pathway markedly diminishes mouse escape behavior and ameliorates fear-related responses. Even in mice with concurrent damage to the cortex and medial amygdala, activation of this pathway remains capable of inducing mouse escape behavior and replicating autonomic nervous response of innate fear. These findings suggest that the identified forebrain-to-hindbrain neural circuit can autonomously regulate TMT-induced innate fear independent of amygdala.Figure 3: Single-cell calcium imaging results of anterior PBNslCck+ positive neurons when TMT is close to the mouse's nose.As a consequence of excessive or repetitive fear contributing to fear-related disorders, such as anxiety, the research team conducted a more in-depth examination of the pathway’s function in anxiety. Dr. WANG Hao stated, “We observed that continuous optogenetic activation of this pathway (1h per day for three days) resulted in markedly observable anxiety-like behaviors in mice. Furthermore, the inhibition of this pathway led to a significant reversal of the anxiety-like behavior after 2h of acute restrain stress.”This study revealed a tetra-synaptic neural circuit of the main olfactory bulb → dorsal peduncular cortex → lateral parabrachial nucleus → parasubthalamic nucleus, and demonstrated that this pathway can regulate olfaction-evoked innate fear and anxiety bypasses the amygdala. Prof. LI Xiao-Ming, the corresponding author of the article, believes that this research not only expands our understanding of the neural mechanisms underlying fear and anxiety but also provides new insights into the pathogenesis of mental disorders.
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  • 11 01
    Social behaviors such as social interaction, recognition and memory are critical for daily life of animals including human beings, and social deficits including social withdraw, anxiety and isolation are closely associated with psychological or neurological disorders1. Therefore, it is important to elucidate the mechanisms of social behaviors.  It has been well known that anterior cingulate cortex (ACC) is a social hub in the brain2, and recent studies demonstrate that hippocampal CA2 pyramidal neurons (PNs) play important roles in social recognition memory3. Binggui Sun’s laboratory in Zhejiang University School of Brain Science and Brain Medicine published a paper in PNAS entitled “Efr3b is essential in social recognition by regulating the excitability of CA2 pyramidal neurons”, providing new insights into the association of CA2 PNs and social behaviors.Efr3 (Eighty-five requiring 3) is the mammalian and yeast homologue of the drosophila rolling blackout (RBO). Previous studies have shown that RBO/Efr3 is important in terms of the phospholipid metabolism at the plasma membrane4. Efr3 includes Efr3a and Efr3b in mammalian cells. Although both Efr3a and Efr3b are highly expressed in the brain, their physiological functions in the brain are largely unknown. We reported previously that deficiency of Efr3a led to increased expression of BDNF and it’s receptor, TrkB5. In the present study, our data of RNAscope in situ hybridization showed that the mRNA of Efr3b was widely expressed in the brain and highly enriched in the hippocampal CA2/CA3 areas. We crossed Nestin-cre mice with Efr3bf/f mice to specifically delete Efr3b in neural cells. Behavioral tests revealed that deficiency of Efr3b in neural cells resulted in impaired social novelty recognition but did not affect the spatial learning and memory, anxiety, fear memory, social interaction and olfactory functions of mice. These phenotypes are very similar with the behaviors of mice after specific inhibition of CA2 PNs reported in a previous study3. Our electrophysiological recordings also showed that the excitability of CA2 PNs was significantly reduced in mice of Efr3b deficiency, suggesting that ablating Efr3b may affect the excitability of CA2 PNs and then impairs the ability of social novelty recognition of mice. To further assess the functions of Efr3b, we specifically knocked down the expression of Efr3b in CA2 PNs via RNAi. We found that reducing Efr3b in CA2 PNs decreased the excitability of CA2 PNs and impaired the social novelty recognition of mice. Interestingly, restoring the expression of Efr3b in CA2 PNs increased their excitability and improved the ability of social novelty recognition in Efr3b-deficient mice. Furthermore, chemogenetic activation of CA2 PNs also improved the social novelty recognition of Efr3b-deficient mice. Collectively, these data indicate that Efr3b is essential in social recognition by maintaining the excitability of CA2 PNs, and deficiency or dysfunction of Efr3b may account for relevant disorders associated with social deficits. Dr. Binggui Sun of Zhejiang University School of Brain Science and Brain Medicine is the leading corresponding author and Drs. Fude Huang and Xuekun Li are co-corresponding authors. Drs. Xiaojie Wei and Jing Wang are the co-first authors of this paper. Yiping Zhang, Enlu Yang and Qi Qian in Binggui Sun’s lab also contribute to this study. This work was supported by grants from National Key Research and Development Program of China (2021YFA1101701, 2019YFA0110103), National Natural Science Foundation of China (31871025, 32071031, 32271028), Natural Science Foundation of Zhejiang Province (LZ19C090001), and the Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences (2023-PT310-01). References1.         Kennedy DP, Adolphs R. The social brain in psychiatric and neurological disorders. Trends Cogn. Sci. 2012, 16: 559-572.2.         Apps MA, et al. The anterior cingulate gyrus and social cognition: tracking the motivation of others. Neuron 2016, 90: 692-707.3.         Hitti FL, Siegelbaum SA. The hippocampal CA2 region is essential for social memory. Nature 2014, 508: 88-92.4.         Baird D, et al. Assembly of the PtdIns 4-kinase Stt4 complex at the plasma membrane requires Ypp1 and Efr3. J Cell Biol 2008, 183: 1061-1074.5.         Qian Q, et al. Brain-specific ablation of Efr3a promotes adult hippocampal neurogenesis via the brain-derived neurotrophic factor pathway. FASEB J 2017, 31:2104-2113. 
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  • 18 12
    The joint research team led by Prof. Xiao-Ming Li and Prof. Yan Zhang has recently published an article entitled Snapshot of the cannabinoid receptor 1–arrestin complex unravels the biased signaling mechanism on Cell online on Dec 14th, 2023. Addressing the long-standing Cannabis problem, an oddity that has vexed scientists for decades, this research achieved a breakthrough by unraveling signaling bias mechanism toward cannabinoid receptor 1 (CB1), facilitating safer synthetic cannabinoid targeting CB1.Over the last ten years, the research team led by Prof. Xiao-Ming Li has been dedicated to identifying key target molecules CB1 in nervous system diseases and developing corresponding treatment strategies, thereby rendering CB1 a promising therapeutic target for pain relief, anti-anxiety, and anti-depression treatment.Cannabis activates CB1, which elicits analgesic and emotion regulation benefits, along with adverse effects, via Gi and β-arrestin signaling pathways. However, the lack of understanding of the mechanism of β-arrestin1 (βarr1) coupling and signaling bias has hindered drug development targeting CB1.Prof. Yan Zhang and his team have been devoted to studying the signaling transduction mechanisms of GPCR in major diseases and have also made substantial contributions to the advancement and establishment of cryo-electron microscopy (cryo-EM)-based GPCR pharmacology. Prof. Xiao-Ming Li, Prof. Yan Zhang and their colleagues have cooperated to determine the 3.1 Å cryo-EM structure of the CB1–βarr1 complex. The availability of high-resolution map facilitates the accurate determination of the binding features of ligand in the CB1–βarr1 structure and reveals notable differences in the transducer pocket and ligand-binding site compared with the Gi-protein complex, a task that has been unachieved in most GPCR–βarr1 complexes characterized at lower resolutions. βarr1 occupies a wider transducer pocket promoting substantial outward movement of the TM6 and distinctive twin toggle switch rearrangements, whereas FUB adopts a different pose inserting more deeply than the Gi-coupled state, suggesting the allosteric correlation between the orthosteric binding pocket and the partner protein site.Taken together, the joint labs led by Professors Li and Zhang have pioneered studies of cannabinoid receptors. Furthermore, this research not only proposes a comprehensive model for the molecular mechanism of signaling bias, but also builds a solid foundation for the development of safer synthetic cannabinoids and the clinical application for the CB1 compounds in treating neurological and psychiatric disorders.Website:
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  • 02 11
       The research team led by Prof. Hao Wang has recently published an article titled “Neural adaption in midbrain GABAergic cells contributes to high-fat-diet induced obesity” in Science Advances.In modern society, high-calorie food is readily available and easily accessible, leading to a steady increase in the incidence of obesity. Obesity, in turn, contributes to the rise of other related diseases such as hypertension, hyperlipidemia, and diabetes, placing a significant burden to both society and families. Consequently, obesity has emerged as a pressing public health concern worldwide, with limited treatment options.While previous studies have demonstrated that weight control can be achieved through modifications in dietary structure and lifestyle habits, it is often observed that individuals in this population tend to regain weight within five years. This phenomenon may be attributed to the impact of high-calorie foods, which not only influence body weight and metabolism, but also induce irreversible changes in the central nervous system. To delve deeper into this issue, Professor Hao Wang and his team from Zhejiang University’s School of Brain Science and Brain Medicine conducted a research study entitled “Neural adaption in midbrain GABAergic cells contributes to high-fat-diet induced obesity”, which was published in Science Advances. The study discussed the neural adaptations observed in midbrain GABAergic cells as a result of high-fat-diet (HFD) induced obesity.Professor Hao Wang's research team has been dedicated to investigating the neural circuit mechanisms involved in regulating energy metabolic homeostasis. In their previous work published in Cell Reports (2019), they made a significant discovery that GABAergic neurons in the ventrolateral periaqueductal grey (vlPAG) region possess an appetite-suppressing effect.In their current study, the team utilized a chemogenetic approach to activate vlPAG GABAergic neurons and observed a reversal of the obesity phenotype in high-fat-diet-induced obese (DIO) mice. This rescue effect was achieved by reducing 24-hour food intake, increasing energy metabolism levels, and inducing browning of adipose tissue.Through the use of in vivo fiber-photometry calcium imaging, the researchers discovered that calcium signals originating from vlPAG GABAergic neurons are suppressed during food intake. Notably, these neurons exhibited stronger suppression in DIO mice. Further electrophysiological recordings provided insights into the mechanisms underlying these observations. The reduced excitability of the "food-suppressed" neurons in obese mice was found to be a result of increased presynaptic inhibitory inputs and a decrease in intrinsic excitability of the neurons themselves. Consequently, chronic high-fat food intake leads to long-term inhibition of these "food-suppressor" neurons, ultimately contributing to increased food intake and obesity.The team further employed single-cell nuclear transcriptome sequencing technology to conduct a comprehensive analysis of gene expression changes in GABAergic neurons within the vlPAG of obese mice, comparing them with control mice. They identified a crucial gene called CACNA2D1, which exhibited significantly reduced expression levels in obese mice. To investigate the potential role of CACNA2D1, the team performed AAV-overexpression of CACNA2D1 in the vlPAG of obese mice. Remarkably, this intervention led to the rescue of the obesity phenotype observed in DIO mice. The rescue effect was achieved by reducing food intake and promoting adipose tissue browning. Additionally, the restoration of CACNA2D1 expression resulted in the recovery of excitability in the "food-suppressor" neurons located in the vlPAG. These findings suggest that CACNA2D1 holds promise as a potential target for the treatment of stubborn obesity.  In summary, Prof. Hao Wang's team found that the "food-suppressor" neurons in the vlPAG are involved in the regulation of energy balance and help maintain body weight homeostasis. However, long-term high-fat food intake will cause these "food-suppressor" neurons to go on strike, which makes the animals unable to stop eating high-fat food, and the vicious cycle of excessive food intake will continue. CACNA2D1 may be a potential target for the treatment of recalcitrant obesity.GABAergic neurons in the periaqueductal grey regulate weight metabolic homeostasis. Professor Hao Wang from the School of Brain Science and Brain Medicine at Zhejiang University served as the corresponding author, while Dr. Xiaomeng Wang and Dr. Xiaotong Wu were the co-first authors of this paper. The study received support from Professor Shumin Duan, Professor Xiaoming Li, Professor Yudong Zhou, Professor Chen Li, Professor Han Xu, Professor Jiadong Chen, Professor Wei Gong, Professor Fang Guo, and Professor Ruimao Zheng. Additionally, Dr. Bingwei Wang, along with PhD students Hao Wu and Hanyang Xiao, made significant contributions to this research. Funding for this study was provided by the National Natural Science Foundation of China and Boehringer Ingelheim in Germany.
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    • Speaker:Yun Li

      Institution:Department of Zoology and Physiology,University of

      Time:2024.5.15 15:00

      Locatiom:Meeting Room 705

      Function and Dysfunction of the Prefrontal Cortex

    • Speaker:Jing Wang

      Institution:Department of Neurobiology, School of Biological S

      Time:May 13, 2024 10:30

      Locatiom:Meeting Room 705

      The Hierarchical Organization of Needs and The Gut’s Influence

    • Speaker:Zhenyu Yue

      Institution:the Center for Parkinson’s disease Neurobiology I

      Time:May 9, 2024 13:30

      Locatiom:Liangzhu Laboratory

      The Landscape of Autophagy in the Brain, Neurological Disorders, ...

    • Speaker:Fan Liu

      Institution:Leibniz Forschungsinstitut für Molekulare Pharmaco

      Time:April 30, 2024 15:30

      Locatiom:Fulou Meeting Room

      Developing structural interactomics and its application in cell bi...

    • Speaker:Volker Haucke

      Institution:Leibniz Forschungsinstitut für Molekulare Pharmaco

      Time:April 30, 2024 14:30

      Locatiom:Fulou Meeting Room

      Lipid switches in cell physiology: From nutrient signals to disea...

    • Speaker:Henry Evrard

      Institution:Shanghai International Center for Primate Brain Re

      Time:2024.4.11 2:00PM

      Locatiom:Meeting Room705

      Functional & Comparative Neuroanatomy of Subjective Feelings

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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】