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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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Impaired spatial memory,anxiety like behavior in a mouse model of sleep deprivation

Impaired spatial memory,anxiety like behavior in a mouse mod...

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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： Afzal Ali MISRANI Li Yang Cheng Long School of Life Science South China Normal University

Sleep deprivation(SD) is a condition that is frequently observed in modern society bringing various neurobehavioral effects, responsible to adversely affect the quality of life. It is more highlighting issue because sleep loss results in learning and memory *** SD and Total SD are the two main techniques that are used to induce stress by SD. REM SD has been shown to adversely affect the cognitive functions and produce anxiety like behavior in rat and mice, but there is no study reported about the total SD and its effects on spatial memory and behavior. In the brain, hippocampus is the main area that is sensitive to stress response and spatial memory is highly dependent on hippocampal formation. Some studies also reported that stress and anxiety can modulate learning and memory. Anxiety is an unpleasant state accompanied by feelings of exaggerated worry, hesitation, fear and pressure. Although the association between sleep and memory is accepted but the basis of these interactions are poorly understood. The aim of this study was to investigate the effects of 24 h total SD on spatial memory and behavior in mice. 3 months old C57 mice were sleep deprived for 24 hours using automated treadmill method. The radial arm maze, a widely used procedure to access both spatial working memory and spatial reference memory, was used to access the memory function. Sleep deprived mice showed impaired reference and working memory. Anxiety behavior was measured using Open field test, force swim test and Plus maze test, extensively used behavioral assessment tasks for this purpose. Mice that were sleep deprived for 24 hours showed reduced locomotor activity and increased immobility time in open field test, indicating anxiety like behavior as compare to control, force swim test results also showed anxiogenic effects in SD mice as it spend more time immobile. SD Mice spent more time in open arms in plus maze test demonstrating anxiogenic behavior. In light of these findings, o

关键词： memory anxiety behavior sleep deprivation

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Changes of dendritic spines and synapses in the process of brain development in APP/PS1 mice

Changes of dendritic spines and synapses in the process of b...

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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： Jing Liu Yu-Juan Shi En-She Jiang Wen-Yi Yan Jin-Bo Deng Dong-Ming Yu Institute of Neurobiology Henan University Institute of Public Hygiene Henan University

Objective Alzheimer's disease(AD) is the most common form of dementia in elderly people. Synapse loss in AD animal models and patients exhibited a close correlation with cognitive deficits. However, the nature and progression of synaptic changes that lead to synapse dysfunction and loss remain to be fully characterized. The dendritic spine is the main structure in the formation of synapse, and its changes in structure and function were viewed as the marker of synaptic plasticity. The present study was to explore the sequence and causality between the age-dependent pathological changes of dendritic spines and synapses and the Aβ gradual accumulation in the brain development in APP/PS1 mice. Methods The hippocampus region of APP/PS1 mice from postnatal day 0 to postnatal day 360 were used as target section. DiI diotistic, immunohistochemistry, and transmission electron microscopy assays were applied to analyze the morphological changes of dendritic spines and synapses in brain tissue. Results(1) Amyloid plaques were observed from P6 m in APP/PS1 mice.(2) The length and density of dendritic spinesin CA1 area of APP/PS1 mice from P3 m were significantly lower than that in wild type mice respectively(P<0.05 and P<0.01).(3) Immunohistochemistrical results showed that the density of synaptophysin from P3 m were significantly reduced(P<0.01), and the synaptic ultrastructure also showed partly abnormalities in APP/PS1 mice. Conclusion The morphology of dendritic spines and synapses exhibited age-dependent changes in APP/PS1 mice and this change occurred earlier than the formation of Aβ plaques. Dendritic spine can be as a better target to evaluate the progress of AD.

关键词： Alzheimer's disease dendritic spine development Aβ hippocampus

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Satellite glial cell P2X7 receptor in rat dorsal root ganglia contributed to visceral hyperalgesia

Satellite glial cell P2X7 receptor in rat dorsal root gangli...

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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： Li-Fang Zou Shuang-Mei Liu Xi Zhang Mo-Feng Ying Qiu-Lan Lv Gui-Lin Li Bing Wu Li-Chao Peng Miao-Miao Song Shang-Dong Liang Department of Physiology Medical School of Nanchang University

Objective Irritable bowel syndrome(IBS) and inflammatory bowel disease often display visceral hypersensitivity. Visceral nociceptors after inflammatory stimulation generate afferent nerve impulses through dorsal root ganglia(DRG) transmitting to the central nervous system. ATP and its activated-P2X7 receptor play an important role in the transmission of nociceptive signal. This study aims to explore whether purinergic signalling is involved in the sensory transmission of visceral pain. Methods Abdominal withdrawal reflex(AWR) was monitored to determine the visceral hyperalgesic sensitivity. P2X7 receptor expression was tested by immunohistochemistry, immunofluorescence, RT-PCR and Western blotting. Results(1) The co-expression levels of P2X7 and glial fibrillary acidic protein(GFAP, a marker of satellite glial cells) in DRG were upregulated in visceral pain rat model.(2) There was abdominal withdrawal reflex(AWR) score in a visceral pain model.(3) After P2X7 antagonist BBG treatment, abdominal withdrawal reflex(AWR) score in a visceral pain model was reduced, the pain threshold was elevated and the co-expression levels of P2X7 receptor and GFAP in DRG were decreased. Conclusion The satellite glial cell P2X7 receptor in rat dorsal root ganglia might be involved in the nociceptive transmission induced by visceral pain.

关键词： Dorsal root ganglia P2X7 receptor Satellite glial cell Visceral hyperalgesia Colorectal distension

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mNGF administration alleviates PTSD symptoms via TrkA/ERK/CREB pathway in a SPS mice model

mNGF administration alleviates PTSD symptoms via TrkA/ERK/CR...

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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： Dayun Feng Jing Yang Baolin Guo Shengxi Wu Department of Neurobiology and Collaborative Innovation Center for Brain Science Fourth Military Medical University Institute of Neuroscience and Anatomy School of MedicineZhejiang University

Posttraumatic stress disorder(PTSD) is an important representation of psychiatric and behavior disorder after stress whose etiology and treatment strategies are not clear to date. Animal models of PTSD like a single prolonged stress(SPS) model are widely used to mimic the PTSD-like symptoms for studying this disease. Nerve growth factor(NGF) is one of the neurotrophic factors(NTs) members who plays a potential role in the development of psychiatric disorders and can be used as drug clinically. In recent study, using mouse SPS model, we investigated the changes of NGF level, neuronal morphology, and several molecules expression involved in NGF signaling pathway in the hippocampus and also explored the possibility of NGF in alleviating the PTSD symptom. Our results showed that the NGF expression reduced at 3d post-SPS(P<0.05) and reached to the lowest level at 14 d post-SPS. Accordingly the decreased level of p-Trk A, p-ERK, p-CREB in the hippocampal tissues was demonstrated by western blotting. Golgi staining showed severe dendrites atrophic changes in the hippocampus and the neuronsdisplayed short and retracted neurites with no neural loss at the SPS-14 d. After administrating 3μg/kg NGF, we found conditioning fear response and anxiety behavior induced by SPS were alleviated. Western blotting results revealed NGF administration led to elevated NGF levels and NGF signal molecular- p-Trk A, p-ERK, p-CREB levels in the hippocampus. Meanwhile administration of NGF rescued SPS-induced atrophy of dendrites of hippocampal neurons and increased expression level of synapsin and PSD95 were also found after NGF administration. Our data demonstrated NGF administration can enhance the formation of synapses and dendrites of hippocampal neurons in SPS mice via activation of ERK/CREB pathway resulting in alleviated PTSD symptom. These findings suggest NGF administration may be a novel therapeutic for PTSD

关键词： NGF PTSD SPS mice model

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In vivo dynamic imaging of subcellular structures in zebrafish Mauthner cell

In vivo dynamic imaging of subcellular structures in zebrafi...

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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： Min Chen Yang Xu Bing HU Laboratory of Neurodevelopment and Repair School of Life SciencesUniversity of Science and Technology of China

Objective Single-cell electroporation is especially useful for studies requiring single cell resolution, such as imaging studies of cell morphology. The ability of single-cell electroporation to co-deliver multiple molecules, including multiple genes to any cell type, makes single-cell electroporation a powerful and versatile method. Unfortunately this powerful tool is rarely used in zebrafish, an excellent model for in vivo imaging. Combining the recent work about PTZ enhances the myelinating capacity of oligodendrocytes and the important role of N-cadherin in axon-oligodendrocyte recognition, we aim to build an in vivo dynamic imaging model of Mauthner cell subcellular structures(N-cadherin) in zebrafish central nervous system by single-cell electroporation and explore the role of N-cadherin in the mechanism of neuronal activity influencing *** Firstly,we optimized the parameters of single-cell electroporation and replaced the expression system to Gal4/UAS system, which maximized the plasmid expressing in zebrafish. Then we labeled the subcellular structures in Mauthner cells by delivering the plasmids CMV-Gal4-VP16 and UAS-Ncad-EGFP using single-cell electroporation. Time-lapse confocal imaging observed the dynamic behaviors of N-cadherin in neuronal axon under physiological and PTZ-treated conditions. Meanwhile, oligopeptides AHAVD was used to block the function of N-cadherin and the influence of PTZ on individual oligodendrocytes myelination was observed. Results(1) In vivo dynamic imaging model of N-cadherin in Mauthner cell was successfully built.(2)N-cadherin-green fluorescent protein(Ncad-GFP) presented obvious differences in their stable accumulations and mobile transports after the treatment of PTZ at the subcellular level.(3)AHAVD can offset the enhancement of PTZ on oligodendrocytes myelination. Conclusion The above results suggest the unique role of N-cadherin involved in the mechanism by which the neuronal activity influencing myelinat

关键词： zebrafish Mauthner cell subcellular in vivo dynamic imaging single-cell electroporation N-cadherin Myelination

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Inhibition of hyperpolarization-activated cyclic nucleotide-gated channels in rat spinal dorsal horn neurons contributes to analgesic effects of lidocaine

Inhibition of hyperpolarization-activated cyclic nucleotide-...

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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： Si-cong Peng Tao Hu Na-na Liu Tao Liu Department of Pediatrics the First Affiliated Hospital of Nanchang University Department of Anesthesiology

The local anesthetic lidocaine has been widely used in surgical anesthesia and pain management by blocking voltage-gated sodium channels. However, growing evidences reveal that blockade of sodium channels cannot account for the full explanation of its analgesic mechanisms. Hyperpolarization-activated cyclic nucleotide（HCN）-gated channel is one of the other possible targets, which is a promising targets for the treatment of pain. Whether lidocaine can inhibit HCN-gated channel current（Ih） in substantia gelatinosa（SG） neurons is currently unclear. By using the whole-cell patch-clamp technique, we investigated the effect of lidocaine on Ih in SG neurons of young rat spinal cord. Peak Ih amplitude decreased right after lidocaine's application, reaching a maximum level within 3 min and gradually subsided within 5～6 min after washout. The inhibition rate of lidocaine on Ih was not significantly different with a second application of lidocaine in the same neuron. There was no change in Ih inhibition when co-applied tetrodotoxin（a Na+ channel blocker） with lidocaine. In addition, lidocaine shifted Ih activation curve in the hyperpolarizing direction by 5.8 m V and increased the time constant over the voltage range from-80 120 m V. Moreover, reversal potential of Ih was shifted to 6.8 m V in negative a delay of the rebound depolarization（RD） onset but also reduced the RD spike frequency. In conclusion, out studies as presented here demonstrate that lidocaine strongly inhibits Ihin SG neurons in a reversible and concentration- dependent way(IC50 inhibition may contribute to suppression of action potential and rebound burst firing frequency. Thus this study provides key insights into a novel cellular mechanism that could be underlying analgesic effects of systemic administration of lidocaine.

关键词： Inhibition of hyperpolarization-activated cyclic nucleotide-gated channels in rat spinal dorsal horn neurons contributes to anal

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Aldosterone induces rapid sodium intake by a nongenomic mechanism in the nucleus tractus solitarius

Aldosterone induces rapid sodium intake by a nongenomic mech...

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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： Hu Qiao Bo Hu Jianqun Yan Hong Zhou Ru Jia Bo Lv Bo Sun Xiao Luo Huiling Sun Limin Guan Xiaojing Wei Yuanyuan Fan Nan Wang Department of Orthodontics Xi’an Jiaotong University School of Stomatology Department of Physiology and Pathophysiology Key Laboratory of Environment and Genes Related to DiseasesMinistry of EducationXi’an Jiaotong University College of Medicine Department of Prosthodontics Xi’an Jiaotong University School of Stomatology Xi’an Jiaotong University School of Stomatology

The purpose of this study was to determine whether aldosterone has a rapid action in the nucleus tractus solitarius(NTS) that increases sodium intake, and to examine whether this effect of aldosterone, if present, is mediated by G protein-coupled estrogen receptor(GPER). Adult male Sprague-Dawley rats(250-300 g) with a stainless-steel cannula in the fourth ventricular(4th V) were used. Aldosterone was injected into the 4th V at the doses of 5, 50, 100, and 200 ng 0.5 μl-1. A rapid dose-related increase of 0.3 M Na Cl intake was induced within 30 min and this increase was not suppressed by the mineralocorticoid receptor(MR) antagonist eplerenone(100 ng 0.5 μl-1). Water intake was not affected by aldosterone. The G protein-coupled estrogen receptor(GPER) agonist G-1(50 ng 0.5 μl-1) produced a parallel and significant increase in sodium intake, while pre-treatment with GPER antagonist G15(100 ng 0.5 μl-1) blocked the G-1 or aldosterone-induced rapid sodium intake. In addition, sodium intake induced by sodium depletion or low-sodium diet fell within 30 min after injection into the 4th V of the MR antagonist eplerenone, while G15 had no effect. Our results confirm previous reports, and support the hypothesis that aldosterone evokes rapid sodium intake through a non-genomic mechanism involving GPER in NTS.

关键词： aldosterone,GPER,nongenomic,nucleus tractus solitarius,sodium intake

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The endpoint of antidepressant treatment in social defeat stress mice associated with BNDF expression in hippocampus

The endpoint of antidepressant treatment in social defeat st...

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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： Xiang-Yu Zhao Jian-Jun Zhang Beijing Key Laboratory of New Drug Mechanisms and Pharmacological evaluation Study Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College

Objective At the preclinical level, the social defeat paradigmis considered one of the most robust models of stress-induced mood-related illnesses which possesses higher face, predictive, and ethological validity that results in enduring behavioral and neurobiological changes that mimic several symptoms of the human condition. In this study,we uesd two antidepressants-duloxetine and fluoxetine to treat social defeat stress depression mice and evaluatd the relatinship between brain-derived neurotrophic factor( BDNF) level in hippocampus and the endpoint of antidepressants therapy. Methods CD1 mice were screened for aggressive behavior following intrusion into their home cages. Those mice exhibiting aggression were used to defeat the C57BL/6 mice. The C57BL/6 mice were defeated for 10 min per day and then housed for the remainder of the day with the aggressor but separated by a plastic divider with holes, where they were exposed to chronic stress in the form of threat for the next 24 *** process was repeated daily for 10 consecutive days with a different CD1 aggressor each day to minimize inter-aggressor *** day 11,defeated C57BL/6 mice were subjected to the social interaction test,only the susceptible mice were equally divided into three groups according the interaction scores to receive vehicle 、duloxetine and fluoxetine treatment for 14 days respectively.24 hours after the last injection mice were subjected to the social interaction test again. Hippocampus were removed for western blotting after the test. Results Fluoxetine but not duloxetine can relieve the depression symptom,the recovery rate come to 87.5%.Western bolt result show that fuloxetine treatment restored the chronic social defeat stress-induced decrease of hippocampal BDNF while duloxetine doesn't have such effect. Conclusion Fluoxetine is effective on social defeat stress depression model while duloxetine isn'*** level of hippocampal BDNF associated with the end point of antidepressant

关键词： depression social defeat stress duloxetine fluoxetine BDNF

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Neuroprotective effects after Brain Extracellular matrix implantation into surgical brain of a TBI mouse model

Neuroprotective effects after Brain Extracellular matrix imp...

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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： Yun Wu Jingwei Zhang Yejie Shi Xiaoming Hu Jun Chen Zhixiong Liu Department of Neurosurgery Xiangya HospitalCentral South University Center of Cerebrovascular Disease Research University of Pittsburgh School of Medicine

Traumatic brain injury(TBI) is a leading cause of death and disability especially in young adult. Extracellular Matrix(ECM) is a potential therapy for brain injuries. ECM provides not only mechanical and structural support to cells and tissues but also binds soluble ligands and transmembrane receptors to provide spatial coordination of signalling processes. In this study, TBI was induced in C57/BL6 mice by a controlled cortical impact(CCI) with a pneumatically driven, 3 mm flat-tip impounder(3.75 m/sec, 150 msec, 1.5 mm depth). Brain Extracellular Matrix(B-ECM) was transplanted into corpus callosum and striatum 1 hour after CCI. Sensorimotor deficits were determined by Rotorod test and Corner test. The time of Rotorod test raised from 175 to 207(range from 0 to 300) and the score of Corner test decreased from 0.39 to 0.20(range from-1 to +1) compared with vehicle-treated mice. Lesion volume was measured 35 days after TBI using MAP-2 immunohistochemical staining. It was also reduced by 31% in ECM treatment group. White matter injury was measured by myelin basic protein(MBP) and neurofilament SMI32(a marker of axonal damage) immunohistochemical staining. The SMI-32/MBP ratio was increased from 14.6 to 7.8 in corpus callosum, 16.2 to 8.3 in striatum region while treated with ECM. Astrocyte activation and scar formation were determined by Glial Fibrillary Acidic Protein(GFAP) peri-lesion site with ECM treatment. In addition, microglia activation were measured byIonized Calcium Binding Adapter Molecule 1(Iba-1) immunohistochemical staining. The number of microglia cells were decreased by 27.3% in ECM treatment group. In sum, Our study suggest that ECM scaffold protein could improve functional outcomes and reduce tissue loss after TBI. In particular, the ECM treatment significantly reduced white matter injury after TBI.

关键词： TBI ECM neurodegeneration neurobehavioral function

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Nppb-expressing Neurons and Their Representative Genes in Primary Sensory Neurons

Nppb-expressing Neurons and Their Representative Genes in Pr...

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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： Dan Wu Chang-Lin Li Hao Luo Yin-Jing Lu Yan-Qing Zhong Lan Bao Xu Zhang Institute of Neuroscience and State Key Laboratory of Neuroscience CAS Center for Excellence in Brain ScienceShanghai Institutes for Biological SciencesChinese Academy of Sciences Institute of Biochemistry and Cell Biology and State Key Laboratory of Cell Biology Shanghai Institutes for Biological SciencesChinese Academy of Sciences

Objective Somatosensory neurons in the dorsal root ganglia(DRG) detect various stimuli and relay the information to postsynaptic neurons in the spinal dorsal horn. DRG neurons are traditionally classified into CGRP-positive peptidergic small-diameter, IB4-labelingnon-peptidergic small-diameter and NF200-positive large-diameter DRG neurons. As technology developed, more methods can be used to identify and explore neuron clusters in detail such as single cell RNA-seq. Our works identified Nppb-positiveneurons as a type of peptidergic small DRG neurons. Here, we intended to identify the representative genes of the Nppb-expressing neurons. Methods The representative genes were screened out by single-cell RNA sequencing. The specific expression of Nppb and other representative genes was identified by single-cell real-time PCR and double-fluorescent in situ hybridization(ISH). Results(1) Nppb-positive neurons contained other representative genes: interleukin 31 receptor A(Il31ra), neurotensin(Nts), somatostatin(Sst) and 5-hydroxytryptamine(serotonin) receptor 1F(Htr1f).(2) Nppb was expressed highly and selectively in one type of small DRG neurons, but lowly expressed in other types of small DRG neurons.(3) Il31 ra, Nts and Htr1 f were predominantly expressed in Nppb-type neurons.(4) Nppb was completely co-localized with Il31 ra in DRG neurons, but not with representative genes of other types of small neurons. Conclusion These results confirmed Nppb-type neurons as an independent type of small DRG neurons.

关键词： dorsal root ganglia(DRG) RNA-sequencing Nppb-expressing neurons representative genes

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