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检索条件"任意字段=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"

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Increased coupling of caveolin-1 and ERα contributes to the Fragile X syndrome

Increased coupling of caveolin-1 and ERα contributes to the...

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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： Qi Yang Ming-Gao Zhao Department of Pharmacology School of PharmacyFourth Military Medical University

Objective: Fragile X syndrome(FXS) is a form of inherited mental retardation in humans that results from expansion of a CGG repeat in the Fmr1 gene. Interaction between estrogen receptor(ER) and lipid raft caveolae is critical for the estrogen signaling. Here, we tested the hypothesis that impaired ER-caveolae coupling contributes to the mental retardation of Fragile X syndrome. Methods: Fmr1 knockout(KO) mouse was used as the model of Fragile X syndrome. Multiple techniques were performed including primary neuronal culture, shR NA interference, western blot, electrophysiological recording, RNA-binding protein immunoprecipitation, RT-PCR, and behavioral tests. Results: In this study, we reported that Glu A1 surface expression and phosphorylation induced by 17β-estradiol(E2) were impaired in the Fmr1 KO neurons. The E2-mediated facilitation of long-term potentiation and fear memory was impaired in the anterior cingulated cortex of Fmr1 KO mice. The increased coupling of caveolin-1(CAV1) and the membrane estrogen receptor ERα under basal conditions contributed to the impairment of ER signaling in Fmr1 KO neurons. FMRP interacted with CAV1 mR NA, and knockdown of CAV1 with sh RNA rescued the synaptic Glu A1 delivery, plasticity, and memory in Fmr1 KO mice. Interpretation: This is the first demonstration that the coupling between ERα and lipid raft CAV1 is critical for the membrane estrogen receptor signaling in synaptic plasticity. Therefore, increased coupling of CAV1 and ERα may elucidate one of the critical abnormal mechanisms for fragile X syndrome.

关键词： Fragile X syndrome estrogen caveolae synaptic plasticity learning and memory

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Novel roles of endocytic protein Numb in mGluR expression and cerebellar motor behaviors

Novel roles of endocytic protein Numb in mGluR expression an...

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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： Liang Zhou De-Juan Wang Dong Yang Jia-Huang Zhou Ya-Jun Xie Hao Huang Ying Shen Department of Neurobiology Key Laboratory of Medical Neurobiology of Ministry of HealthZhejiang University School of Medicine Institute of Developmental and Regenerative Biology College of Life and Environmental ScienceHangzhou Normal University

Objective Numb is first identified as a cell fate determinant in drosophila and is essential for maintaining neural stem cells during neurogenesis and promoting neuronal development. Nevertheless, the function of Numb in mature neurons has not been *** 1 metabotropic glutamate receptor(mGluR1) is highly expressed in Purkinje cells(PCs) and plays critical roles in cerebellar long-term depression(LTD) and motor behaviors. Although the downstream signaling of mGluR1 has been investigated, a key question is that the regulatory mechanism of mGluR1 is unclear. Methods Western blots, in situ hybridization, single cell RT-PCR, confocal imaging, whole-cell recording, and behavioral studies were performed in control and conditional Numb knockout mice. Results Synaptic m Glu R1 was significantly reduced in mutant mice. In contrast, AMPA receptors were unchanged in mutant PCs, suggesting the effect of Numb may be specific to m Glu R1. Moreover, transient and persistent forms of mGluR1 plasticity and the expression of mGluR1-associated genes and proteins were investigated in mutant mice, and our results showed that loss of Numb in PCs did not affect mGluR1 plasticity and the levels of mGluR1-related proteins. Nevertheless, Numb deficiency inhibited the intracellular trafficking of mGluR1 upon agonist stimulation in slices. Conclusion Numb is a novel regulator for mGluR1 expression and transport.

关键词： Numb mGluR1 long-term depression Purkinje cell cerebellum

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Role of interleukin-17 in cerebral ischemic injury and its molecular mechanism in mice with ischemic stroke

Role of interleukin-17 in cerebral ischemic injury and its m...

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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： Jinling Yu Shujuan Li Song Han Ting Liu Junfa Li Department of Neurobiology Beijing Institute for Brain DisordersCapital Medical University Department of Neurology Capital Medical University Affiliated Beijing Chaoyang Hospital

To explore the dynamic change of interleukin-17A(IL-17A)in cerebrospinal fluid(CSF) and blood after ischemic stroke in vivo. Futher, to observe whether there are some nerve cells involved in the secretion of IL-17 A, which impact on neuronal ischemic injury and potential molecular mechanism. By establishing mouse cerebral artery occlusion(MCAO) model and cortical primary neurons after oxygen-glucose deprivation(OGD) model, and using enzyme-linked immunosorbent assay(ELISA), 3-(4,5- dimethyl-thiazol-2)-2,5-diphenyl tetrazolium bromide(MTT) assay, immunofluorescence and western blot. These methods were used to detect the level of IL-17 A in blood and cerebrospinal fluid, primary neuron injury, IL-17A-positive cells colocalize with other cells, and the related proteins about damage pathway. A significately increased was detected at 24 h after MCAO and peak at 3 day. However, IL-17 A in CSF are only increased at 12 h after MCAO. In the vitro model, cortical primary neurons after oxygen-glucose deprivation(OGD), recombination IL-17A(rI L-17A) can aggravate neuronal injury neuronal injury. Cortical neurons derived from IL-17 A knockout mice expressed higher level of autophagy and apoptosis compared with wild-type mice after OGD treatment. IL-17 A after ischemic stroke increases in the blood and cerebrospinal fluid, and it plays an important role in aggravating neuronal injury through autophagy and apoptosis pathways.

关键词： interleukin-17 ischemic stroke oxygen-glucose deprivation(OGD)

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Research of firing characteristic of “VL-cortical SMA” in rat during fatigue exercise

Research of firing characteristic of “VL-cortical SMA” in ...

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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： Lijuan Hou Mengyu Wang Xiaoli Liu Decai Qiao Exercise Physiology Lab Beijing Normal University

Background: Ventrolateral thalamus(VL) is located between the rear and front of ventromedial hypothalamic nucleus. It receives the output from different parts of basal ganglia(BG), also known as the "last channel" of basal ganglia motion-control information. Supplementary motor area(SMA) is an important part of the motor cortex. Our previous research involved in "basal ganglia- thalamo- cortical" pathway's function in the possible mechanisms of exercise-induced fatigue. We found exhaustive situation can break this balance, which may be derived from the excessive activation of the basal ganglia output nuclei and downstream output excessive suppression inhibition of neurotransmitter. In order to reveal the central mechanism of exercise-induced fatigue, this research records the neuron activity after different intervention in SMA and VL. Methods: Male wistar rats were randomly divided into a control group and fatigue group. We selected treadmill incremental exercise program to establish exercise-induced fatigue model. Glass microelectrodes technique was selected to record the VL spontaneous activity and local field potentials(LFP) of SMA. Results:(1) Fatigue exercise increased VL neurons proportion of type discharge, reduce discharge rules and a single cluster of neurons in the proportion of electricity paid, but the total discharge frequency decreased.(2) Fatigue exercise reduced the overall discharge frequency of SMA LFP, energy distribution and decreased the excitability of the SMA.(3) During the fatigue condition, the average total power has been significantly improved, δ wave significantly lower, while the proportion of θ wave, α wave, β and γ wave has significantly increased. Conclusions: This study demonstrated that exhaustive exercise mainly reduced the VL excitability, affected the excitatory of "VL-SMA" pathway. It can influence the signal transduction during and after exercise-induced fatigue(31171138/31401018)(5142012).

关键词： central fatigue lateral ventral nucleus supplementary motor area local field potential

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Clustering of Self-Motion Selectivity in the ventral intraparietal (VIP) area of rhesus monkey

Clustering of Self-Motion Selectivity in the ventral intrapa...

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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： Mengmeng Shao Aihua Chen Key laboratory of Brain Functional Genomics (Ministry of Education & Science and Technology Commission of Shanghai Municipality) Primate Research CenterEast China Normal University

Clustering of functional properties is a prominent feature of the cortex, which may play an important role in processing the particular stimulus parameters. Neurons in the ventral intraparietal area(VIP) show directionally selective responses to both visual(optic flow) and vestibular stimuli. VIP is thought to play an important role during multisensory self-motion perception and the neurons are expected to show clustering according to their direction preferences. However, the clustering of these response characteristics is not known. In the current study, single units(SUs) were isolated with a dual voltage-time window discriminator on-line. Multiunit activity(MU) from the same microelectrode was obtained by off-line processing of the digitized raw neural signal, then further compared with the relevant SUs. The strength of 3D spatial tuning was computed with a direction discrimination index(DDI). The DDI values of MU(mean: 0.54 ? 0.0057 SE,vestibular;0.57 ? 0.0060 SE,visual) and SU(mean: 0.60 ? 0.0052 SE,vestibular;0.64 ? 0.0060 SE,visual) were significantly correlated for both vestibular(r=0.34;p<0.0001) and visual(r=0.51;p<0.0001) conditions. For 32% had significant tuning for both SUs and MU responses for vestibular, we computed the smallest angle in 3D between the preferred direction vectors for SU and MU activity. The distribution of |?preferred direction| had peaks close to 0?. Similar results were observed in visual condition. Overall, our results show that the local directional preferences is well clustered in VIP, providing implications for how visual and vestibular signals regarding self-motion may be decoded from populations of VIP neurons.

关键词： ventral intraparietal cortex self-motion selectivity vestibular visual

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Impaired cortical neurogenesis in Plexin-B1 and-B2 doubledeletion mutant

Impaired cortical neurogenesis in Plexin-B1 and-B2 doubledel...

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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： Karen Chen Nicolas Daviaud Yong Huang Roland H.Friedel Hongyan Zou Department of Neurosurgery Icahn School of Medicine at Mount Sinai

Mammalian cortical expansion is tightly controlled by fine-tuning of proliferation and differentiation of neural progenitors in a region-specific manner. How extrinsic cues interface with cell-intrinsic programs to balance proliferative versus neurogenic decisions remains an unsolved question. We examined the function of Semaphorin receptors Plexin-B1 and-B2 in corticogenesis by generating double mutants, whereby Plexin-B2 was conditionally ablated in the developing brain in a Plexin-B1 null mutant background. Absence of both Plexin-Bs resulted in cortical thinning, which wasmore prominentin thecaudomedial cortex. Plexin-B1/B2 double, but not singlemutants exhibited a reduced neural progenitor pool, attributable to less proliferation and an altered division mode favoring cell cycle exit. This resulted in deficient production of neurons throughout the neurogenic period, proportionally affecting all cortical laminae. Consistent with the in vivo data, cultured neural progenitors lacking both Plexin-B1 and-B2 displayed decreased proliferative capacity and increased spontaneous differentiation. Our study therefore defines a novel function of Plexin-B1 and-B2 as extrinsic regulators to maintaina proliferative and undifferentiated state of neural progenitors. Since single mutants display no apparent cortical defects, we conclude that Plexin-B1 and-B2 play redundant or compensatory roles during forebrain development to ensurecorrect neuronal production and neocortical expansion.

关键词： Impaired cortical neurogenesis in Plexin-B1 and-B2 doubledeletion mutant

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Expressions of aquaporin family in cultured astrocytes of Wistar rat

Expressions of aquaporin family in cultured astrocytes of Wi...

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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： Fang Yuan Zhong-Fang Shi Li-Xin Xu Li-Ping Dong Xu Yan Shao-Hua Yang Department of Pathophysiology Beijing Neurosurgical InstituteBeijing Tiantan HospitalCapital Medical University Department of Pharmacology and Neuroscience University of North Texas Health Science Center

Since the molecular mechanism underlying cerebral edema is not clear, the treatment of cerebral edema has remained unchanged for the past 90 years. Recent studies have showed that aquaporin 4(AQP4) is highly expressed in astrocytes and plays important role in brain edema, but whether other aquaporin(AQP) subtypes are also expressed in astrocytes is unknown. The purpose of this study is to explore AQP family(AQP1-11) expressions in astrocytes. One-day-old Wistar rats were used for astrocyte culture and the purity of cultured cells was determined by the immunocytochemical stain with glial fibrillary acidic protein. The real-time fluorescent quantitative PCR was used to examine the expressions of AQP1-11 on the 9th day of primary culture. We detected the expressions of AQP1, 3, 4, 5, 7, 8, 9, and 11 in the cultured astrocytes, but no expressions of AQP 2, 6. The expression level of AQP4 was the highest, followed by AQP1, AQP11, AQP9 and AQP5. It is noteworthy that the expression level of AQP4 was thirty times as much as that of AQP1. These results suggested that AQP4 is the major AQP in astrocytes and play a key role in brain edema and the roles of other AQPs(including AQP1, AQP11, AQP9 and AQP5) in brain edema is also worthy of further study.

关键词： aquaporin astrocyte,cell culture

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Differential alterations in the morphology and electrophysiology of layer II pyramidal cells in the primary visual cortex of a mouse model prenatally exposed to LPS

Differential alterations in the morphology and electrophysio...

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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： Ying Gao Li-Xiong Liu Qi-Qin Li Yun Wang School of Optometry and Ophthalmology and Eye Hospital and Key Laboratory of Visual ScienceNational Ministry of HealthWenzhou Medical University Genesys Research Institute Tufts University

Maternal inflammation is a known risk factor for schizophrenia and autism. Since the visual processing has shown abnormalities in these disorders, we explored whether neuropathologic changes can be caused in the primary visual cortex in offsprings due to the maternal inflammation induced by a single lipopolysaccharide（LPS） injection in pregnant mouse dams. The morphology and electrophysiological properties of layer II pyramidal cells（L2PC） in the primary visual cortex were investigated with whole-cell patch-clamping recording and 3D neuron reconstruction techniques. Although the composition of two L2 PC types was unchanged, a reorganization of the dendritic architecture was found in both L2PC and L2PC types, predominantly in the L2PC type, of the mice prenatally exposed to LPS. Moreover, prenatal LPS exposure differentially altered intrinsic electrophysiological properties of the two L2 PC types. L2PC neurons showed reduced excitability as featured by a hyperpolarization of the resting membrane potential, whereas L2PC neurons showed enhanced excitability as featured by a decrease in cellular input resistance at resting membrane potential. These significant changes in neuronal morphological and electrophysiological properties might contribute to the dysfunctions of pyramidal neurons after maternal inflammation.

关键词： Lipopolysaccharide Morphology Intrinsic electrophysiological properties Layer Ⅱ pyramidal neuron Primary visual cortex Patch clamp

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Optogenetic manipulation of spatial attention and working memory in the nonhuman primate

Optogenetic manipulation of spatial attention and working me...

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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： Ji Dai David L.Sheinberg Institute of Psychology Chinese Academy of Sciences Department of Neuroscience Brown University

In the nonhuman primate, area LIP is thought to be a key neural substrate for visual attention and working memory. To explore the functional contribution of neural activity in this region, we artificially activated LIP neuron by optogenetic activation, a technique that allows temporally precise control on genetically targeted neurons. In two behavioral experiments, the viral construct AAV5-Ca MKIIa-C1V1（E122T/E162T）-TS-EYFP was used to induce green light sensitivity. In the first study, monkeys were trained to perform avisuospatial discrimination task, in which they were required to choose a target by making a saccade to a ‘T' and not a ‘+' distractor. We found that optogenetic activation could systematically bias choices and speed responses for targets presented at the receptive field location（Dai et al., 2014）. In another spatial working memory experiment, we trained the monkeys to memorize the location of a shortly presented cue, then, following a go cue, saccade to the target presented at the same location but not a distractor presented elsewhere. Optogenetic stimulation was applied randomly either at the visual cue phase, during the memory phase, or at the saccade execution phase. Our data indicate that when the cue was presented at the receptive field of neurons near the stimulation site and the distractor was presented 45 o counterclockwise away, optogenetic activation during the execution phase impaired performance by 0% and increase reaction times by 0ms. These effects were accompanied by a higher frequency of uncertain saccades. Weaker effects were observed for stimulation at the cue encoding and memory phase. Together, in addition to demonstrating the utility of optogenetics in modulating behavior in a primate model, these results also strongly support that area LIP plays a central role in visual attention and in direct execution of saccadic eye movements.

关键词： optogenetics primate attention working memory

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System for whole mouse brain mapping of neurocircuits with single neuron resolution

System for whole mouse brain mapping of neurocircuits with 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： Hui Gong Shaoqun Zeng Xiangning Li Jing Yuan Anan Li Qingming Luo Britton Chance Center for Biomedical Photonics Wuhan National Laboratory for Optoelectronics-Huazhong University of Science and Technology

The brain is the most sophisticated, complex and significant organ in the bodies of humans and other higher organisms. The study of neural circuits that distributed in the brain through neurites, i.e. axons and dendrites, is essential to understanding how the brain operates when healthy, injured or diseased. However, current knowledge about the intricate patterns of neural circuits is extremely sparse. For investigating these distributions, it would be ideal not only to be able to visualize neural circuits consisting of local and long-distance connections at single neuron resolution in a entire mouse brain but also achieve the neuron location information simultaneously. In this presentation, we introduce a fluorescence wide-field large-volume tomography method. Combined with block sectioning, a fast and robust and high precision fluorescence imaging was achieved by a structuredillumination microscopy. We also introduced a novel resin-embedding method optimized for fluorescent protein labelled mouse brain to provide both adequate specimen hardness and fluorescence intensity. With these techniques, we acquired two colors whole brain datasets of an 8-week-old C57BL/6J mouse injected of the adeno-associated virus vector plasmid(AAV, expressing GFP) into the cingulate cortex(Cg) with voxel size of 0.32× 0.32 × 2 ?m3 in 3 days. We could not only show a group of axonal projection pathways, but also discovered a new axonal long-distance projection from a neuron oriented in the Cg. With advanced labelling techniques, our method is believed to open an avenue to exploring both local and long-distance neural circuits and cell types that are related to brain functions and brain diseases down to the neurite level.

关键词： microscopic optical imaging,whole brain,neural circuit,axon

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