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Galectin-9 is increased during neuroinflammation and promotes remyelination

Galectin-9 is increased during neuroinflammation and promote...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Steelman,A.J. Lu,H.C. Kim,S. Hernandez,J. Zhou,B. Li,J Laboratory of Immunophysiology and Behavior Department of Animal SciencesUniversity of Illinois Department of Veterinary Integrative Biosciences Texas A&M UniversityCollege Station

Objective Multiple sclerosis(MS) is an inflammatory and neurodegenerative disease of the central nervous system that causes substantial morbidity. Galectins are carbohydrate binding proteins that are capable of modulating immune responses. Galectin-9 is increased in the brains of MS patients, but its contribution to the natural history is unknown. Methods We utilized galectin-9 null(Lgals9-/-) mice to investigate the contribution of galectin-9 to inflammatory demyelination during experimental autoimmune encephalomyelitis(EAE) and cuprizone- and lysolecithin-induced de/remyelination. Results(1) Galectin-9 is increased in the CNS during EAE and cuprizone intoxication and localizes to macrophages/microglia and astrocytes.(2) Compared to control mice Lgals9-/-mice displayed heightened EAE severity which was associated with increased neuropathology and infiltration of MOG-specific Th17 cells.(3) Glial-derived galectin-9 did not influence the effector function or viability of Th17 cells in culture.(4) The absence of galectin-9 expression was associated with delayed remyelination.(5) Immunohistochemical analysis of the lesions revealed that Lgals9-/- mice have similar numbers of total(olig2+) oligodendrocytes, but a reduced number of mature(CC1+) oligodendrocytes compared to controls.(6) Treatment of primary mixed glial cultures with recombinant galectin-9 promoted oligodendrocyte maturation. Conclusion In response to inflammation galectin-9 becomes upregulated within the CNS, where it promotes repair.

关键词： Multiple sclerosis galectin-9 neuroinflammation EAE cuprizone remyelination

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Proteomic Profiling of Aging Hippocampus from a Postmortem Human Brain Bank

Proteomic Profiling of Aging Hippocampus from a Postmortem H...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Benhong Xu Yanpan Gao Wenying Qiu Tao Wang Naili Wang Di Zhang Wei Ge Chao Ma Institute of Basic Medical Sciences Neuroscience CenterChinese Academy of Medical SciencesSchool of Basic MedicinePeking Union Medical College

Hippocampus is one of the most critically affected regions in aged human brain. However, aging-related changes in protein profile in the human hippocampus have not been well described, especially for the Chinese population. We performed a proteomic study in the postmortem human hippocampus from the Human Brain Bank in Chinese Academy of Medical Sciences and Peking Union Medical College. A total of 16 human brains were used and divided to 4 aging groups: 20-50, 50-70, 70-90, and over 90(n=4 each). None of the donors were diagnosed with neurodegenerative diseases before death according to their medical history. TMT-labeled quantitative protein profiling methods were applied and the results identified 4582 proteins, among which 99 proteins were upregulated and 42 proteins were downregulated during the aging process. Bioinformatics analysis revealed a numbers of proteins involved in the cytoskeletal or electron transport chain were significantly changed in aged hippocampus as compared to the younger groups. However, proteins highly associated with AD such as APP and tau showed no significant change in aged brains. Some of the proteins significantly changed during the aging process were verified by western blot. This study demonstrated the feasibility of research based on a standardized human brain bank in China. Our results indicated a series of changes in proteomic profile in aged human hippocampus that may relate to the normal aging process and potentially against age-related neurodegenerative disorders.

关键词： aging,human brain bank,brain proteomics,hippocampus

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Regulation of cPKCγ on phosphorylation status of synapsin-I and their role in cerebral ischemia/hypoxia injury

Regulation of cPKCγ on phosphorylation status of synapsin-I...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Hongyi Zhu Nan Zhang Jie Zhong Dan Zhang Song Han Junfa Li Department of Neurobiology and Beijing Institute for Brain Disorders Capital Medical University Department of Anatomy Capital Medical University

Previously, we have reported that conventional protein kinase C(cPKC)g was involved in the protective effect of mouse cerebral hypoxic preconditioning(HPC). In addition, we further identified some c PKCg-interacting proteins, including synapsin-I in the cortex of HPC mice by using proteomics approach. In the present study, by using c PKCg knockout(c PKCγ-/-) mice, we further explored the regulatory effect of cPKCg on synapsinco-immunoprecipitation and Western blot in oxygen-glucose deprivation(OGD)-induced ischemic model of primary cultured cortical neurons. In addition, we also applied immunofluorescence to examine the influence of cPKCg knockout on synaptic morphology after OGD-induced primary cortical neurons injury. Co-immunoprecipitation results indicated that c PKCγ could interact with synapsin-I in the cerebral cortex of mice. OGD insults significantly reduced phosphorylation of synapsin-I at Ser549 and Ser553, while the knockout of cP KCg further decreased synapsin-I phosphorylation(n=6, p<0.05 compared with Normoxia). OGD treatment also decreased the length and number of neurites of primary cultured cortical neurons, and cPKCγ-/- group worsened the damage of synaptic morphology induced by OGD(n=6, p<0.05 compared with Normoxia). In summary, c PKCγ could regulate the phosphorylation status of synapsin-I at Ser549 and Ser553, thereby influent the function of synapsin-I on neurite growth in ischemic/hypoxic injury.

关键词： oxygen-glucose deprivation(OGD) conventional protein kinase C(cPKC)γ Synapsin-I knockout

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Characterize the potentialroles of autism-related genes in sleep behavior

Characterize the potentialroles of autism-related genes in s...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Huawei Tong Qian Li Junhai Han Institute of Life Sciences the Key Laboratory of Developmental Genes and Human DiseaseSoutheast University

Autism spectrum disorders(ASD) are characterized by some core features, including markedly abnormal or impaired social interaction and communication, restricted interests, and stereotypical behaviors. In addition to these core diagnostic features, children with ASD frequently present with a host of associated behavioral issues, such as sleep problems. Numerous studies have indicated that children with ASD experience more sleep problems than the general population. These sleep disturbances primarily include delayed sleep onset, frequent waking in the night, early morning waking, and decreased total sleep time. However, the reason of sleep disturbances in children with ASD is largely *** that sleep is regulated genetically and the regulation of sleep are highly conserved from fly to humans, we used Drosophila as a genetic model to investigate the potential roles of ASD-related genes in sleep behavior. We showed that lost-of-function of some ASD-related genes resulted in sleep deficits. Neuroligins and Neurexins are cell adhesion molecules involved in synapse formation and function, and mutations in neuroligin and neurexin genes are linked to ASD. Previously, we have shown that neuroligin 4 mutant flies exhibited the prolonged sleep onset and the reduced night sleep time, and we revealed that Neuroligin 4 regulates sleep through modulating GABA transmission. Here, we showed that neurexin mutant flies exhibited the defective sleep maintenance and the advanced arousal. We revealed that Neurexin bi-directionally regulates sleep behavior through regulating synaptic transmission in the different region of mushroom body. Our study reveals the unknown mechanism of Neurexin in modulating synaptic transmission and in regulating sleep behavior, and offers insights into the mechanism of sleep disturbances in autism patients.

关键词： ASD Characterize the potentialroles of autism-related genes in sleep behavior

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Triptolide promotes α-synuclein degradation in neuronal cells by autophagic pathway

Triptolide promotes α-synuclein degradation in neuronal cel...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Ting Zhang Guanzheng Hu Le Wang Yang Liu Xiaomin Wang Department of Neurobiology Capital Medical UniversityBeijing Institute for Brain Disorders and Key Laboratory for Neurodegenerative DisorderMinistry of Education

Parkinson's disease(PD) has become a social problem in China, seriously affecting population health and life quality and inhibiting economic development. However, no effective treatment for PD is available to control the disease progression. Our previous study shows that triptolide provides neuroprotective effect in different animal models of PD, but the mechanism is still unclear. In the present study, we transfected wild-type(WT) or A53 T mutant(A53T) α-synuclein in MN9 D cells for 24 h and added different concentrations of triptolide for another 24 h. We found triptolide reduced α-synuclein overexpression level in MN9 D cells. To test whether triptolide reduced the synthesis of α-synuclein, we observed the m RNA level of α-synuclein by RT-PCR assay and found triptolide has no effect, indicating triptolide promoted the degradation of α-synuclein. Considering the autophagy-lysosome pathway(ALP) and the ubiquitin-proteasome system(UPS) are both involved in the α-synuclein recycling, we added 3-MA, an inhibitor of autophagy, and lactacysin, an inhibitor of proteasome with triptolide and found 3-MA, but not lactacysin, abolished the inhibition effect of triptolide. Moreover, the level of p62 declined with α-synuclein expression, indicating autophagy machinery is involved in this process. These results provide the first evidence that triptolide may promote the clearance of α-synuclein inneuronal cells, which may help translate the application of triptolide from bench to bedside, as well as to advance our understanding of alternative medicine in the treatment of PD.

关键词： triptolide,autophagy,α-synuclein

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Calorie restriction attenuates cerebral ischemic injury via increasing SIRT1 synthesis in the rat

Calorie restriction attenuates cerebral ischemic injury via ...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Ming-zi Ran Zhao-ju Li Lu-jia Yang Li Tong Li-na Zhang Hai-long Dong Department of Anesthesiology Xijing HospitalFourth Military Medical University Department of Anesthesiology General Hospital of Guangzhou Military Command of PLA Department of Anesthesiology Chinese PLA General Hospital

Caloric restriction(CR) has been shown to have several health benefits and provides protection against type 2 diabetes, neurodegenerative and cerebral vascular diseases. It reduces the brain infarct size and promotes neurological functional recovery after cerebral ischemia. Sirtuin 1(SIRT1) plays an important role in the biological effects induced by CR. This study investigated the role of SIRT1 in ischemic tolerance in the brain induced by CR. Sprague drawly rats were divided into two groups based on food intake. Ad libitam(AL) group was fed with normal diet while the CR group received 60% calories compared to AL. All animals were subjected to a middle cerebral artery occlusion for 90 min. Results showed the neurological function score of CR group was higher and the brain infarct volume was markedly reduced in CR group compared to AL group at 24 h after reperfusion( p <0.05). CR increased the synthesis of SIRT1 significantly(p <0.05), and ameliorated the down regulation of SIRT1 expression at 6 and 12 h after middle cerebral artery occlusion(p <0.05, p <0.01, respectively). Knockdown of SIRT1 by si RNA in vivo reversed the neuroprotective effect of CR. From this study, we deduce that CR induces brain ischemic tolerance on rats via increasing the synthesis of SIRT1.

关键词： Calorie restriction SIRT1 Brain ischemic tolerance Neuroprotection

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Ginkgo Biloba extract(EGb 761) attenuates lipopolysaccharide-induced inflammatory responses in N9 microglia by blocking the NF-kappaB pathway

Ginkgo Biloba extract(EGb 761) attenuates lipopolysaccharide...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Guo-Hong Wang Ying Wang Na Li Chao-Kun Li Hong-Gang Zhao Dong-Liang Li Department of Physiology and Neurobiology Xinxiang Medical University College of Chemistry and Life Science Guangdong University of Petrochemical Technology The Third Affiliated Hospital of Xinxiang Medical University

Microglial activation and microglia-mediated neuroinflammation play an important role in the pathogenesis of numerous neurological diseases. Gingko biloba extract EGb761 has been widely used in China and Europe for the treatment of ischemia, stroke, dementia and neurodegenerative diseases. In the present study, the effects of EGb761 on lipopolysaccharide(LPS)-induced microglial activation and inflammatory responses were investigated. N9 microglial cells were pretreated with EGb761 for 1 h prior to stimulation with LPS. The cell viability, nitric oxide(NO) production, the expression of inducible nitric oxide synthase(iN OS), interleukin-1beta(IL-1β) and tumour necrosis factor-alpha(TNF-α), and nuclear translocation of nuclear factor kappa B(NF-κB) p65 subunit were evaluated. Our results showed that EGb761 effectively reversed LPS-induced morphological changes without causing cytotoxity, and significantly inhibited LPS-induced production of NO, IL-1β and TNF-α. Moreover, the m RNA expression of i NOS, IL-1β and TNF-α in response to LPS was also down regulated by EGb761. In addition, EGb761 remarkably reduced the nuclear translocation of NF-κB p65 subunit in LPS-stimulated N9 microglial cells. In conclusion, EGb761 is able to inhibit LPS-induced microglial activation and inflammatory responses by blocking the NF-κB signaling pathway. Therefore, EGb761 may be a potential candidate for the treatment of microglia-mediated neuroinflammatory diseases.

关键词： EGb 761 microglia LPS neuroinflammation NF-κB

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TRPV1 and PLC involved in histamine H4 receptor induced reaction on mouse DRG neurons

TRPV1 and PLC involved in histamine H4 receptor induced reac...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Tun-Yu Jian Niu-Niu Yang Yan Yang Chan Zhu Jin-Ao Duan Guan-Yi Wu Zong-Xiang Tang College of Basic Medicine Nanjing University of Chinese Medicine

Histamine H4 receptor has been recognized to play a role in evoking peripheral pruritus. However, the ionic and intracellular signaling mechanism of activation of H4 receptor on the dorsal root ganglion(DRG) neuron is still unknown. By using cell culture and calcium imaging, the underlying mechanism of activation of H4 receptor on the DRG neuron was studied. Application of immepip dihydrobromide(8.3-50 μM), a histamine H4 receptor special agonist, could induce dose dependent increasing in intracellular Ca2+([Ca2+]i) of DRG neurons. 77.8% immepip dihydrobromide-sensitized DRG neurons also respond to the TRPV1 high selectively agonist capsaicin. On the other hand, immepip dihydrobromide-induced response of DRG neuron was blocked by N-ethylmaleimide, an antagonist of G-protein. Perfusing DRG neurons with PLC pathway antagonist U73122, could block the activation of H4 receptor by immepip dihydrobromide-induced. In addition, the immepip dihydrobromide-induced increasing [Ca2+]i could be blocked by uthenium red and capsazepine respectively, while could not be blocked by TRPA1 antagonist HC-030031. These results indicate that TRPV1 but not TRPA1 is the important ion channel to induce DRG neurons responses in downstream signaling pathway of histamine H4 receptor, and suggest TRPV1 may involve in the mechanism of histamine-induced itch response by H4 receptor activated.

关键词： Histamine H4 receptor TRPV1 PLC

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The structural connectivity pattern of the default mode network and its association with memory and anxiety

The structural connectivity pattern of the default mode netw...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Yan Tao Bing Liu Xiaolong Zhang Jin Li Wen Qin Chunshui Yu Tianzi Jiang Brainnetome Center Chinese Academy of Sciences National Laboratory of Pattern Recognition Institute of AutomationChinese Academy of Sciences Department of Radiology Tianjin Medical University General Hospital Queensland Brain Institute The University of Queensland Key Laboratory for Neuro Information of Ministry of Education School of Life Science and TechnologyUniversity of Electronic Science and Technology of China

The default mode network(DMN) is one of the most widely studied resting state functional networks. The structural basis for the DMN is of particular interest and has been studied by several researchers using diffusion tensor imaging(DTI). Most of these previous studies focused on a few regions or white matter tracts of the DMN so that the global structural connectivity pattern and network properties of the DMN remain unclear. Moreover, evidences indicate that the DMN is involved in both memory and emotion, but how the DMN regulates memory and anxiety from the perspective of the whole DMN structural network remains unknown. We used multimodal neuroimaging methods to investigate the structural connectivity pattern of the DMN and the association of its network properties with memory and anxiety in 205 young healthy subjects. With the probabilistic fiber tractography technique based on DTI data, we constructed the global structural connectivity pattern of the DMN and found that the DMN has a definite structural basis. Using the graph theory method, we found that memory was significantly positively correlated with the efficiency of the DMN whereas anxiety was found to be negatively correlated with the efficiency. This study provides evidence for a significant role that the DMN plays in memory and anxiety, offering a perspective at the network level that showed that a higher level of memory corresponded to a higher efficiency of the DMN network, while a higher level of anxiety corresponded to a lower efficiency.

关键词： DTI DMN memory anxiety structural network

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Coordinated spine pruning and maturation mediated by inter-spine competition for cadherin/catenin complexes

Coordinated spine pruning and maturation mediated by inter-s...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Wen-Jie Bian Wan-Ying Miao Shu-Ji He Zilong Qiu Xiang Yu Institute of Neuroscience State Key Laboratory of NeuroscienceCAS Center for Excellence in Brain ScienceShanghai Institutes for Biological SciencesChinese Academy of Sciences University of Chinese Academy of Sciences

Dendritic spines are postsynaptic compartments of excitatory synapses that undergo dynamic changes during development, including rapid spinogenesis in early postnatal life and significant pruning during adolescence. Spine pruning defects have been implicated in developmental neurological disorders such as autism, yet much remains to be uncovered regarding its molecular ***, we showed that spine pruning and maturation in the mouse somatosensory cortex are coordinated via the cadherin/catenin cell adhesion complex and bidrectionally regulated by sensory experience, i.e. accelerated by environmental enrichment(EE) and blocked by whisker deprivation. We further demonstrated usinglive imaging in cultured neurons that locally enhancing cadherin/catenin-dependent adhesion or photo-stimulating a contacting channelrhodopsin-expressing axon stabilized the manipulated spine and eliminated its neighbors, an effect requiring cadherin/catenin-dependent adhesion and depending on the inter-spine ***, when we overexpressed β-catenin in a subset of presynaptic axons in the mouse somatosensory cortex, thusdifferentiating the level of cadherin/catenin-dependent adhesion between neighboring spines of the same postsynaptic neuron in vivo, we observed enhanced survival of the spine contacting the β-cateninoverexpressing axon, at the expense of its β-catenindeprived neighbor. Thus, we demonstrated,both in vitro and in vivo,that inter-spine competition for cadherin/catenin complexesbiased spine fate. Finally, both EE-induced acceleration of spine pruning and spine maturation were abolished in the absence of endogenous β-***, these results suggest that activity-induced inter-spine competition for β-catenin provides specificity for concurrent spine maturation and elimination, and thus is critical for the molecular control of spine pruning during neural circuit refinement.

关键词： sensory experience spine pruning spine maturation cadherin/catenin complex inter-spine competition

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