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检索条件"任意字段=长三角地区神经科学论坛2016暨第八次会员代表大会"

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SUMO-specific protease 1 Protects Neurons from Apoptotic Death during transient brain ischemia/reperfusion

SUMO-specific protease 1 Protects Neurons from Apoptotic Dea...

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长三角地区神经科学论坛2016暨第八次会员代表大会

作者：李勇上海交通大学医学院基础医学院

SUMO-specific protease 1（SENP1） deconjugates SUMO from modified proteins. Although post-ischemic activation of SUMO conjugation was suggested to be neuroprotective against ischemia/reperfusion（I/R） injury, the function of SENP1 in this process remained unclear. Here we show that transient middle cerebral artery occlusion（t MCAO） in mice followed by 6, 12 and 24 h reperfusion significantly enhanced SENP1 levels in the affected brain area, independent of transcription. Consistent with the increase in SENP1, the levels of SUMO1-conjugated proteins were decreased by I/R in cortical neurons of wild type mice, but unchanged in that of animals with conditional ablation of SENP1 gene from adult principal neurons, the SENP1flox/flox;Cam KII-cre（SENP1 c KO） line. The SENP1 c KO mice had a significant increase in infarct volume in cerebral cortex and more severe motor impairment in response to I/R as compared to the wild type littermates. Cortical neurons from I/R injured SENP1 c KO mice became more apoptotic than wild type neurons, as indicated by both TUNEL staining and caspase-3 activation. Overexpression of SENP1 in somatosensory cortices of adult wild type mice suppressed I/R-induced neuronal apoptosis. We conclude that SENP1 plays a neuroprotective role in I/R injury by inhibiting apoptosis through decreasing SUMO1 conjugation. These findings reveal a novel mechanism of neuroprotection by protein desumoylation, which may help development of new therapies for mitigating brain injury associated with ischemic stroke.

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Optogenetic activation of medial septal cholinergic neurons during slow-wave sleep disrupts hippocampal ripple oscillations

Optogenetic activation of medial septal cholinergic neurons ...

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长三角地区神经科学论坛2016暨第八次会员代表大会

作者：林龙年 Key Laboratory of Brain Functional Genomics (Ministry of Education) Institute of Brain Functional Genomics School of Life Science East China Normal University

Existing pharmacological and lesion data indicate that acetylcholine(ACh) plays a crucial role in memory acquisition and consolidation. Elevated ACh release from the cholinergic basal forebrain enhances memory acquisition during waking, while low levels of ACh mediates memory consolidation during slow-wave sleep(SWS). We identified firing patterns of medial septal(MS) cholinergic neurons and thire physiological functions in freely behaving Ch AT-Ch R2-EYFP transgenic mice with multichannel in vivo recording and optogenetic techniques. In the medial septum of Ch AT-Ch R2-EYFP transgenic mice, confocal microscope immunohistochemistry showed that Ch R2-YFP-labeled somata were almost all cholinergic: 98.5 ± 3.4% of Ch R2-YFP-labeled somata were Ch AT-positive, and of Ch AT-activity of positive somata, 75.4 ± 14.9% were labeled with Ch R2-YFP. We recorded the activities of the MS cholinergic neurons that responded to blue light stimulation. Most of the MS cholinergic neurons showed high theta-related activity. It is because these cells fired more spikes during the theta states of exploration and rapid eye movement sleep. On the other hand, their activity level stayed low during the non-theta states of quiet waking and slow-wave sleep. Interestingly, optogenetic activation of MS cholinergic neurons during slow-wave sleep could completely disrupt ripple oscillations in hippocampal CA1 region. Pharmacology revealed that this inhibitory effect of MS cholinergic neurons on ripple could be blocked by atropine, an antagonist of muscarinic cholinergic receptors. These results suggest that the reason why Ach can block SWS-related consolidation of memory is that high levels of hippocampal Ach during SWS can suppress hippocampal sharp-wave ripple via muscarinic receptors.

关键词： medial septum acetylcholine hippocampus memory consolidation ripple oscillations

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Somatosensory Neuron Types Identified by High-Coverage Single-Cell RNA-Sequencing and Functional Heterogeneity

Somatosensory Neuron Types Identified by High-Coverage Singl...

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长三角地区神经科学论坛2016暨第八次会员代表大会

作者：李昌林 Kai-Cheng Li Dan Wu Yan Chen Hao Luo Jing-Rong Zhao Sa-Shuang Wang Ming-Ming Sun Ying-Jin Lu Yan-Qing Zhong Xu-Ye Hu Rui Hou Bei-Bei Zhou Lan Bao Hua-Sheng Xiao Xu Zhang Institute of Neuroscience and State Key Laboratory of Neuroscience CAS Center for Excellence in Brain Science Shanghai Institutes for Biological Sciences Chinese Academy of Sciences School of Life Science and Technology Shanghai Tec University National Engineering Center for Biochip at Shanghai Shanghai Clinical Center Chinese Academy of Sciences/Xu Hui Central Hospital State Key Laboratory of Cell Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences

Sensory neurons are distinguished by distinct signaling networks and receptive characteristics. Thus, sensory neuron types can be defined by linking transcriptome-based neuron-typing with the sensory phenotypes. Here, we classified somatosensory neurons of the mouse dorsal root ganglion(DRG) by highcoverage single-cell RNA-sequencing(10,950 ± 1,218 genes per neuron) and neuron size-based hierarchical clustering. Moreover, single DRG neurons responding to cutaneous stimuli were recorded using an in vivo whole-cell patch-clamp technique and classified by neuron-type genetic markers. Small-diameter DRG neurons were classified into one type of low-threshold mechanoreceptor and five types of mechanoheat nociceptor(MHN). Each of the MHN types was further sorted into two subtypes. Large DRG neurons were categorized into four types, including neurexophilin 1-expressing MHNs and mechanical nociceptors(MNs) marked by BAI1-associated protein 2-like 1(Baiap2l1) expression. Mechanoreceptors marked by trafficking protein particle complex 3-like and Baiap2/1-marked MNs were further clustered into two subtypes each. These results provide a new system for cataloging somatosensory neurons and their transcriptome databases.

关键词： DRG Somatosensory Neuron Types Identified by High-Coverage Single-Cell RNA-Sequencing and Functional Heterogeneity RNA Neuron

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Synaptic preservation associated with CD36/EEA1-induced clearance of amyloid-β by macrophages

Synaptic preservation associated with CD36/EEA1-induced clea...

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长三角地区神经科学论坛2016暨第八次会员代表大会

作者：李松林 David A Daley Yosef Koronyo Eric Y Hayden Dieu-Trang Fuchs Julia Sheyn Altan Rentsendorj Tania Torbati Keith L Black David B Teplow Koronyo-Hamaoui Maya The institute of Life Sciences Wenzhou University Department of Neurosurgery Maxine-Dunitz Neurosurgical Institute Cedars-Sinai Medical Center Department of Neurology David Geffen School of Medicine at UCLA and Mary S. Easton Center for Alzheimer's Disease Research at UCLA Brain Research Institute and Molecular Biology Institute University of California

Synaptopathy is tightly associated with cognitive impairments in Alzheimer’s disease（AD）. Oligomers of the 42-residue long amyloid β-protein（Aβ42） may be key synaptotoxic agents. Enhanced cerebral recruitment of Aβ-clearing macrophages, achieved by glatiramer acetate（GA） immunization, or by blood grafted CD115+-monocytes, leads to attenuation ofcognitive decline in AD mouse models. We measured the impact of defined and stabilized Aβ42oligomers on synaptic integrity, while also assessing synaptic preservation by macrophages and GA treatment（to enhance phagocytosis）. We found that primary cortical neurons exhibit a conformation-dependent susceptibility to Aβ42 fibrils, and more so, to oligomers;bothtriggered neuritic retraction and massive loss of pre-VGlu T1 and post-PSD95 synaptic density. Coculturing primary neurons with GA-treated macrophages substantially protected against these effectsby enhancing CD36-scavenger receptor and early endosome antigen（EEA1）-mediated macrophage clearance of Aβ42 assemblies. GA-treated macrophage media showed increased extracellular degradation of Aβ42, particularly of oligomers. Comprehensive analysis of entorhinal cortex and hippocampal substructures in APPSWE/PS1ΔE9 transgenic mice indicated significant synaptic loss, which was reversed by GA immunization and grafted CD115+-monocytes. Synaptic preservation correlated with retained cognition and reduced cerebral Aβ. Our data suggest that GA inducesneuroprotective macrophage responses, possibly through enhanced CD36/EEA1-mediated clearance of synaptotoxic Aβ42 fibrils and oligomers.

关键词： Alzheimer’s disease Synapse Neurodegeneration Neuropathology Immunotherapy Aβ Amyloid astrogliosis Immune modulation Regeneration Innate Immune cells

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FGF13A-mediated epigenetic regulation of neurogenesis in the developing mouse brain

FGF13A-mediated epigenetic regulation of neurogenesis in the...

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长三角地区神经科学论坛2016暨第八次会员代表大会

作者：周嘉伟 Yingqi Zhai Wei Li Jiawei Zhou Institute of Neuroscience Shanghai Institutes for Biological Sciences Chinese Academy of Sciences

FGF13 is known to be a non-secretory protein of the fibroblast growth factor（FGF） family which is enriched in brain during development and is correlated with two kinds of non-systematically X-linked mental retardation, suggesting its important roles in mental development of human. Previous studies have shown that FGF13 B, one of FGF13 isoforms, is a regulator for microtubule assembly during axonal outgrowth and migration of immature neuron. However, the biological function of FGF13 during brain development remains poorly understood. Toward this end, we generated Fgf13 gene conditional knockout（c KO） mice by crossing FGF13-floxed mice with either nestin-Cre ERT2 or h GFAP-Cre mice targeting neural stem cells / progenitors. We found progressively decreased neurogenesis in the hippocampal subgranular zone of Fgf13 c KO mice at various stages of development. In vitro cultured Fgf13-null neural stem cells also showed dramatic impairment in the ability to proliferate and self-renew. Interestingly, FGF13 A, which is known as the only nuclear isoform of FGF13, contributed more significantly to this phenotype. Yeast-two-hybrid screening identified FGF13 A as an interacting protein with AT Rich Interactive Domain 1B（ARID1B）, a protein that is known to function as a subunit of SWI/SNF chromatin remodeling complex, and is also associated with human mental retardation diseases. FGF13 A was able to maintain the expression of ARID1 B. Taken together, our data suggest that FGF13 functions as an important regulator in the maintenance of neurogenesis in the developing brain. FGF13 A is an uncharted component of the SWI/SNF chromatin remodeling complex, providing new insights into the molecular mechanisms of brain development.

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Down-regulation of progranulin improve learning and memory in a mice model of fragile x syndrome through TNFR2/NFκB pathway

Down-regulation of progranulin improve learning and memory i...

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长三角地区神经科学论坛2016暨第八次会员代表大会

作者：张鹍 Yujiao Li Kaiyin Zheng Qi Yang Le Yang Xinshang Wang Shimeng Zhou Chao Zhang Qian Song Shuibing liu Yumei Wu Minggao Zhao Department of Pharmacology School of Pharmacy Fourth Military Medical University Center for Neuron and Disease Frontier Institutes of Life Science and of Science and Technology Xi'an Jiaotong University

Fragile X syndrome（FXS） is the most common inherited cause of autism and intellectual disability only after Down’s syndrome, caused by the loss of fragile X mental retardation protein FMRP, a RNA-binding protein regulating translation and transportation. By now it is short of effective treatment. We sought out perturbing progranulin（PGRN）, a key TNFα blocker and neurotrophin, as an effective treatment for FXS model mice. We found higher levels of PGRN in FMR1 knock out（KO） mice than in wild type（WT） mice. Moreover excessive PGRN will lead defects in dendritic spine pruning and LTP expression without affecting LTD. As PGRN can directly bind to two TNFα receptors, it important to detect the roles of two TNFRs in LTP. We proved activation of TNFR2 but not TNFR1 is necessary for LTP expression. In further research we found that PGRN could activate TNFR2 directly, and then increased NFκB and p-Glu R1（ser845/831） levels which couldn’t further be elevated after chemical LTP induction, uncovering a ceiling LTP disability produced by excessive PGRN. In addition, knocking down PGRN correct abnormal signal pathways, immature dendritic spine morphology and multiple behavioral phenotypes, including fear memory deficits, hyperactivity, and behavioral inflexibility through interfering TNFR2/NFκB pathway. Basing on our research we found that partially blocking TNFR2/ NFκB pathway using JSH-23, a small chemical molecule, was a good treatment for FXS. Our results support the PGRN as a novel treatment target for FXS, and broaden our understanding of neurotrophins in neurodevelopment.

关键词： fragile X syndrome progranulin TNFα TNFR2/NFκB pathway

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IL-1β knock-down in the hippocampus alleviates lipopolysaccharide-induced memory deficits, depression-and anxiety-like behavior in mice

IL-1β knock-down in the hippocampus alleviates lipopolysacc...

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长三角地区神经科学论坛2016暨第八次会员代表大会

作者： Chenli Li Mengmeng Li Jiacheng Geng Xiongxiong Cai Hanjie Yu 王闯 Qingwen Wang Ningbo Key Laboratory of Behavioral Neuroscience Zhejiang Provincial Key Laboratory of Pathophysiology School of Medicine Ningbo University

Peripheral inflammatory responses affect central nervous system（CNS） function, the main symptoms involve memory deficits, depression and anxiety. Interleukin-1β（IL-1β）, a proinflammatory cytokine, has been proposed to be a key mediator in a variety of behavioral actions of stress. The objective of this study was to explore the involvement of Nrf2 and biochemical alterations of inflammatory or oxidative stress markers in the alleviating effects of IL-1β knock-down on lipopolysaccharide-induced memory deficits, depression-and anxiety-like behavior in mice. The mice were treated with either IL-1β-RNAi lentivirus（1μg/side） or vehicle lentivirus（1μg/side） by microinjection into CA1 subregions of hippocampus. After 7 days recovery, LPS（1 mg/kg, i.p.） or saline were administrated. The behavioral tests for memory deficits were conducted on novel object recognition test（NORT）, and for the depression-like behaviors were performed by sucrose preference test（SPT） and forced swim test（FST） and for the anxiety-like behaviors were examined by zero maze in mice. Furthermore, expressions of Nrf2 were examined by western blotting, and the inflammatory factors（IL-1β and TNF-α） and the brain-derived neurotrophic factor（BDNF） were assayed by ELISA kit. The oxidative stress markers of malonaldehyde（MDA）, SOD and nitric oxide（NO） were performed by commercial colorimetric kit assays. Our results demonstrated that IL-1β knock-down significantly attenuated LPS-induced memory deficits, depression-like and anxiety-like behaviors in mice. In addition, IL-1β knock-down ameliorated LPS-induced neuroinflammation responses by reducing IL-1β and TNF-α levels in hippocampus. Further, IL-1β knock-down also prevented LPS evoked oxidative stress via restored brain pro-oxidant/anti-oxidant balance by inhibiting MDA, SOD and NO concentrations. Finally, we also confirmed that IL-1β knock-down reversed the downregulation of Nrf2 induced by LPS. In conclusion, our results may suggest that co-morbid depressio

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Gambierol inhibition of voltage-gated potassium channels augments spontaneous Ca2+ oscillations in cerebrocortical neurons

Gambierol inhibition of voltage-gated potassium channels aug...

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长三角地区神经科学论坛2016暨第八次会员代表大会

作者：曹征宇 State Key Laboratory of Natural Medicines Department of Complex Prescription of Traditional Chinese Medicine China Pharmaceutical University

Gambierol is a marine polycyclic ether toxin produced by the marine dinoflagellate Gambierdiscustoxicus andis a member of the ciguatoxin toxin family. Gambierol has been demonstrated to be either a low efficacy partial agonist/antagonist of voltage-gated sodium channels or a potent blocker of voltage-gated potassium channels(Kv). Here we examined the influence of gambierol on intact cerebrocortical neurons. We found that gambierol producedboth a concentration-dependent augmentation of spontaneous Ca2+ oscillations, and aninhibition of Kv channel function with similar potencies. Additionally, an array of selective as well as universal Kv channel inhibitors mimicked gambierol in augmenting spontaneous Ca2+ oscillations in cerebrocortical neurons. These data are consistent with a gambierol blockade of Kv channels underlying the observed increase in spontaneous Ca2+ oscillation frequency. We also found that gambierol produced a robust stimulation of ERK1/2 phosphorylation. Gambierol-stimulated ERK1/2 activation was dependent on both inotropic(N-methyl-D-aspartate, NMDA) and type I metabotropic glutamate(m Glu) receptors inasmuch as MK-801(NMDA receptor inhibitor) and S-(4)-CPG as well as MTEP(type I m Glu R inhibitors) attenuated the response. In addition, 2-APB, an IP3 receptor inhibitor, and U73122, a PLC inhibitor, both suppressed gambierol-induced ERK1/2 activation further confirming the role of type I m Glu R mediated signaling in the observed ERK1/2 activation. Finally, we found that gambierol produced a concentration-dependent stimulation of neurite outgrowth that was mimicked by 4-AP, a universal potassium channel inhibitor. Considered together these data demonstrate that gambierol alters both Ca2+ signaling and neurite outgrowth in cerebrocortical neurons as a consequence of blockade Kv channels.

关键词： Gambierol inhibition of voltage-gated potassium channels augments spontaneous Ca oscillations in cerebrocortical neurons

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海洋药物芋螺毒素及其受体研究进展

海洋药物芋螺毒素及其受体研究进展

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长三角地区神经科学论坛2016暨第八次会员代表大会

作者：长孙东亭朱晓鹏吴勇胡远艳李晓丹罗素兰海南大学热带生物资源教育部重点实验室-海口市海洋药物重点实验室

热带特有药用海洋动物芋螺分泌产生的芋螺毒素,在国际上被誉为"海洋药物宝库",它们具有特异结合动物体内各种离子通道和受体的特殊功能。芋螺毒素具有多样化的三维结构而被认为是微小蛋白质,其种类多、活性强、选择性高,已跃... 详细信息

热带特有药用海洋动物芋螺分泌产生的芋螺毒素,在国际上被誉为"海洋药物宝库",它们具有特异结合动物体内各种离子通道和受体的特殊功能。芋螺毒素具有多样化的三维结构而被认为是微小蛋白质,其种类多、活性强、选择性高,已跃居动物毒素研究的首位,已成为当今神经科学研究和新药研发的热点。其中的α-家族芋螺毒素能特异性地作用于乙酰胆碱受体（n ACh Rs）,对其亚型具有空前的选择性阻断活性。n ACh Rs介导众多中枢和外周神经系统的生理功能,包括学习、记忆、成瘾、应答、镇痛和运动控制等。我们海南大学多年来一直从事海南产芋螺毒素及其受体的研究,发现了6个海南产新颖α*-芋螺毒素,对它们的人工合成、三维结构、作用靶点、与受体相互作用机制、药理药效等进行了深入研究。来自海南产织锦芋螺的α-芋螺毒素Tx IB,是目前国际上唯一能将α6/α3β2β3亚型与其他所有n ACh Rs亚型区分开的配体物质和新化合物,并且α6/α3β2β3 n ACh Rs是治疗烟瘾和毒瘾的新型药物作用靶点。来自海南产织锦芋螺的另一新型α-芋螺毒素Tx ID,是迄今为止国际上发现的活性最强的α3β4 n ACh Rs亚型的选择性阻断剂,其半阻断剂量只有12.5 n M。新近发现,α3β4 n ACh Rs介导小细胞肺癌的发生,以及细胞变异和癌细胞的生长,有可能是具有恶性转移特性的小细胞肺癌的新靶点。来自海南产疣缟芋螺的α-芋螺毒素Lv IA,能区分α3β2及其非常接近的α6/α3β2β3亚型,是对人类α3β2和α6/α3β2β3 n ACh Rs相似亚型区分度最好的配体。从海南产菖蒲芋螺中发现了αB-新超家族芋螺毒素Vx XXIVA,是α9α10乙酰胆碱受体的阻断剂。从海南产信号芋螺中发现了结构独特的α-芋螺毒素Lt IA,作用于α3β2 n ACh R上的新的微位点。更加引人关注的是,从海南产将军芋螺中发现了αO-新家族芋螺毒素Ge XIVA,是迄今为止国际上活性最强的特异阻断α9α10乙酰胆碱受体的芋螺毒素,其半阻断剂量只有3.8 n M,且是国际上首个具有电压依赖性的α9α10 n ACh R特异阻断剂。存在于外周神经系统的α9α10 n ACh Rs不仅是治疗神经痛的药物靶点,还是癌症化疗、乳腺癌、肺癌、伤口愈合等的新靶点,可以通过肌肉注射途径给药发挥镇痛活性。Ge XIVA在CCI神经痛模型上的镇痛活性比吗啡强000倍,还具有神经保护和修复功效,且不成瘾,肌肉注射给药途径方便,不会影响运动功能,安全性好。有关Ge XIVA的研究成果已申请中国、美国、欧洲和日本专利,并在国际著名杂志PNAS上发表。

关键词：乙酰胆碱受体海南产α*-芋螺毒素结构与功能神经受体药理学

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