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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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Cutaneous Neurogenic Inflammation at the Sensitized Acupoints induced by Gastric Mucosal Injury in Rats

Cutaneous Neurogenic Inflammation at the Sensitized Acupoint...

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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： Wei He Xiao-Yu Wang Hong Shi Wan-Zhu Bai Bin Cheng Ling Hu Mei-Ling Wu Yang-Shuai Su Zhao-Kun Yang Xiao-Chun Yu Xiang-Hong Jing Bing Zhu Institute of Acupuncture and Moxibustion China Academy of Chinese Medical Sciences The Affiliated Hospital Shandong University of Traditional Chinese Medicine

In acupuncture practice, the most important step is to confirm the location of a sensitized acupoint which reflects a diagnosis and can be stimulated with a specialized needle to treat the disease. Abnormal symptoms such as hyperalgesia or allodynia at the sensitized acupoints in patients with visceral disorders are considered to be in relation with referred pain and neurogenic inflammation. Yet, limited study has investigated the cutaneous neurochemical changes of the sensitized acuponits. The resent study developed an animal model of gastric mucosal injury(GMI) by HCl administered into the stomach of the rats. Evans Blue(EB) dye was applied by injection of tail vein after mucosal damage to observe the neurogenic plasma extravasation dots in the skin of the rats. The EB dots extravagated in the skin were compared with locations of acupoints. Immnohistochemistry analysis was used to detect the expression of calcitonin gene-related peptide(CGRP)- or substance P(SP)-labeled nerve fibers, histamine(HA)-, serotonin(5-HT)-, and tryptase-labeled cells in EB dots. Images were recorded and analyzed by Confocal imaging system and Olympus Image Processing Software. The results showed that GMI resulted in neurogenic plasma extravasation in the skin of the acupoints over the back and abdomen, which mostly occurred in the T9-11 dermatomere. The EB extravasation dots appeared after GMI and disappeared gradually during the natural self-recovery of the gastric mucosa. More SP and CGRP positive nerve fibers were distributed in EB dots than in regions besideEB dots and in the control, mostly distributed in the nerve fibers around both the vessels and root of hair follicle. Mast cells also aggregated and degranulated to release algogenic substances of 5-HT and HA around the vessels in areas of the EB dots. Our results indicates that the mechanism of EB extravasation in the skin of the acupoints are closely related to neurogenic inflammation induced by GMI and that the high expression

关键词： Gastric Mucosal Injury,Sensitized Acupoints,Nociceptive Neuropeptide,Mast Cell,HA,5-HT

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Lipid binding is required for normal subcellular distribution and surface targeting of acid-sensing ion channel 1a

Lipid binding is required for normal subcellular distributio...

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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： Di-Shi Liu Xing-Lei Song Michael Xi Zhu Tian-Le Xu Department of Anatomy and Embryology Department of Biochemistry and Molecular Cell BiologyInstitute of Medical SciencesShanghai Jiao Tong University School of Medicine Department of Integrative Biology and Pharmacology University of Texas Health Science Center at Houston

Acid-sensing ion channel(ASIC) is a family of cation channels that are activated by extracellular p H reduction. Subunit 1a(ASIC1a) is widely expressed throughout the neural system and has been reported to contribute to many pathological conditions, including ischemic cell death and pain. We showed previously that regulated surface insertion of ASIC1 a is important for central sensitization development in peripheral inflammatory pain(Duan et al, J Neurosci, 2012) while ASIC1 a internalization regulates acid-induced cell death(Zeng et al, J Neurosci, 2013), implicating the critical role of membrane trafficking in the channel function. Here, we examined the cellular and molecular mechanisms that underlie ASIC1 a trafficking. We found the cytoplasmic C-terminus of ASIC1 a to be essential for its binding to membrane lipids and normal surface localization. A di-arginine motif in juxtamembrane region of the C-terminus is critical for these two processes through binding to anion phospholipids, especially phosphatidylserine(PS). Mutating the arginines to neutral or negatively charged residues disrupted the binding between ASIC1 a C-terminus and PS and decreased surface expression of full-length ASIC1 a without affecting the total protein expression level and channel assembly, suggesting the importance of electrostatic interaction between ASIC1 a and PS in membrane targeting of the channel. Furthermore, ASIC1 a and PS are well colocalized not only on the surface membrane but also in intracellular organelles as shown by fluorescence confocal microscopy. Together, we have identified a positively charged di-arginine motif in ASIC1 a C-terminus that binds to phospholipids. This electrostatic interaction between the lipid and channel may be an important control step of ASIC1 a trafficking.

关键词： acid-sensing ion channel 1a phospholipids trafficking

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FMRP regulates NGF-induced axon elongation by targeting axonal Map1b and Calm1 in primary sensory neurons

FMRP regulates NGF-induced axon elongation by targeting axon...

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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： Bin Wang Lin Pan Man-Yi Wei Qiang Wang Nuo-Xin Wang Xing-Yu Jiang Xu Zhang Lan Bao State Key Laboratory of Cell Biology Institute of Biochemistry and Cell BiologyShanghai Institutes for Biological SciencesChinese Academy of Sciences National Center of Nanoscience and Technology Institute of Neuroscience and State Key Laboratory of Neuroscience CAS Center for Excellence in Brain ScienceShanghai Institutes for Biological SciencesChinese Academy of Sciences

Objective Axonal localization of mR NAs and translation are important for axon elongation. Fmr1-encoded protein, FMRP, as a RNA-binding protein(RBP), has been suggested playing a central role in dendritic mR NA targeting, stability and subsequent translation. However, the role and mechanism underlying precisely control of axonal translation by FMRP in axon development is not extensively explored. Here, our study is to investigate the role and mechanism of FMRP in the axon development of primary sensory neurons. Methods The association between FMRP and its targets including transcripts of MAP1B(Map1b) and calmodulin(Calm1) was detected by RNA Co-IP experiment. The FMRP-mediated axonal transport of Map1 b and Calm1 and axon elongation were performed by live-cell imaging. Results(1) FMRP was associated with Map1 b and Calm1 in the axons of primary sensory neurons.(2) Knockdown of FMRP decreased axonal level and transport of Map1 b and Calm1 as well as protein level of MAP1 B and calmodulin in axons(3) Knockdown of FMRP impaired NGF-induced axon elongation by suppressing axonal translation of MAP1 B and calmodulin. Conclusion FMRP regulates NGF-induced axon elongation by locally targeting Map1 b and Calm1 in primary sensory neurons.

关键词： FMRP mRNA local translation axon elongation

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Potential therapeutic targets for Alzheimer's neurodegeneration

Potential therapeutic targets for Alzheimer's neurodegenerat...

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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： Wang Jian-Zhi Department of Pathophysiology Key Laboratory of Ministry of Education of China for Neurological DisordersTongji Medical CollegeHuazhong University of Science and Technology

Alzheimer's disease is the most common cause of neurodegeneration in the elderly. Since cholinergic deficit and excitatory amino acid toxicity are the well recognized pathologies in the Alzheimer's brain, the correlated clinical drug treatments mainly include cholinesterase inhibitors and N-methyl-D-aspartate receptor(NMDAR) antagonist. However, both types of drugs can only moderately improve the symptoms but cannot cure the disease, or even delay the disease progression. Therefore, it is in urgent need to search for new drug targets. By using tau hyperphosphorylation, beta-amyloid production, morphological and functional synapse impairments as readouts, our group has demonstrated that glycogen synthase kinase 3?(GSK-3?) and protein phosphatase-2A(PP2A) play a crucial role in Alzheimer's neurodegeneration. We found that GSK-3? can phosphorylate tau while PP2 A dephosphorylate tau at multiple Alzheimer-associated sites. Inhibition of PP2 A arrests neuronal axon outgrowth and knockdown of PP2 A endogenous proteinaceous inhibitor attenuates tau hyperphosphorylation and amyloid accumulation. Upregulation of GSK-3? inhibits long-term potentiation with suppression of presynaptic vesicle exocytosis by phosphorylating P/Q-type calcium channel and interrupting SNARE complex formation. Phosphorylation of tau by GSK-3? promotes reciprocally tau SUMOylation, which inhibits tau ubiquitination and prohibits tau degradation. GSK-3? activation aggrevates beta-amyloid-induced neuronal damages, inhibits PP2 A, and mediates the olfactory deficit-induced hippocampal impairment. The disease-modified GSK-3? intervention arrests the pathology and memory deficits in an Alzheimer's animal model. Our studies provide new insights for the crucial role of GSK-3? in Alzheimer's neurodegeneration and memory impairment, which also shed light for potential intervention.

关键词： glycogen synthase kinase 3? protein phosphatase-2A Alzheimer's disease neurodegeneration

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Administration of COG1410 Reduces Aβ deposition and ameliorates cognitive deficits after traumatic brain injury in Mice

Administration of COG1410 Reduces Aβ deposition and amelior...

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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： Junling Gao Ying Cui Wenqian Zhang Ran Li Xiaohua Jiang Yanxia Tian Kaijie Wang Jianzhong Cui School of Basic Medical Science North China University of Science and Technology Hebei Key Laboratory for Chronic Diseases Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases Department of Surgery Hebei Medical University

Traumatic brain injuryas a cause of progressive neurodegenerative disorders and display Alzheimer's disease(AD)-like cognitive impair- *** is solid evidence that traumatic brain injury(TBI) is a risk factor for AD and disturbances of the balance between production and degradation of amyloid beta(Aβ) certainly play a crucial role in the *** mortem analysis of brains of long-term survivors as well as patients surviving only few days after a brain trauma demonstrated a widespread deposition of Aβ peptides. The TBI-induced up-regulation of Aβ*** measuring Aβ after experimental TBI in rat, we found that Aβ peaked early after injury(12-48 hours). Although the role of Aβin the injury cascade is unknown, multiple preclinical studies have demonstrated a correlationbetween reduced Aβ and improved cognitive outcome. Therefore, therapeutic strategies that enhance Aβ clearance may be beneficial after TBI. COG1410, a synthetic peptide derived from the apolipoprotein E(apo E) receptor binding region, has anti-inflammatory effects after experimental TBI, with improvements in cognitive recovery. However, the effects of COG1410 on Aβ is not known. The current study evaluated the effects of 1 mg/kg daily COG1410 versus saline administered intravenously starting 30 min after TBI on *** found that treatment with an COG1410 reduces the TBI-induced A β peak at(12-48) *** the same time Aβ related inflammatory cytokines IL-1β and TNF-α can also be *** biochemical changes are accompanied by improvements in congnitive functional outcome and a reduction in brain lesion volume. These data suggest that COG1410 is neuroprotective in TBI models of central nervus system(CNS) *** studies are needed to investigate the underlying mechanisms, therapeutic time window,and physiological implications of this effect.

关键词： traumatic brain injury,cognitive function,COG1410,Aβ,inflammatory response

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Opotogenetic activation of adenosine A2A receptor signaling in the dorsomedial striatopallidal neurons suppress goal-directed behavior

Opotogenetic activation of adenosine A2A receptor signaling ...

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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 Li Yan He Mozi Chen Li Chen Ping Li Bo Li Haiyan Li Zhili Huang Zhihui Li Jiang-Fan Chen The Institute of Molecular Medicine School of Optometry and Ophthalmology and Eye HospitalWenzhou Medical University Department of Pharmacology Fudan University Shanghai Medical College Molecular Biology Center Research Institute of Surgery and Daping HospitalThird Military Medical University Department of Neurology Boston UniversitySchool of MedicineBostonMassachusettsUnited States of America

Striatum plays an essential role in neural control of goal-directed and habitual behavior to achieve optimal performance of task. Adenosine A2A receptors(A2ARs) with enriched expression in the striatum modulate instrumental learning, but the contributions of the striatopallidal A2ARs in dorsolateral(DLS) and dorsomedial striatum(DMS) to the control of instrumental learning are not defined. To address whether the transient activation of the striatopallidal A2AR in DMS and DLS precisely at the time of reward was sufficient to modulate instrumental learning, we have developed the rhodopsin-A2AR chimeras(opto-A2AR) and demonstrated that transient light activation of A2AR signaling in the striatopallidal neurons in a "time-locked" manner precisely at the time of reward did not affect instrumental learning at the acquisition or extinction phases, but was sufficient to change animal's sensitivity to outcome devaluation. Specifically, optogenetic activation of striatoapllidal A2AR signaling in DMS suppressed goal-directed behaviors while focally genetic knockdown of striatopallidal A2ARs in DMS enhanced goal-directed behavior by the devaluation test. By contrast, optogenetic activation or focal AAV-Cre-mediated knockdown of striatopallidal A2AR in DLS had little effect on instrumental learning. Thus, the striatopallidal A2AR signaling in DMS exerts inhibitory control of goal-directed behavior by acting precisely at the time of reward, and may represent a therapeutic target to reverse abnormal habit formation that is associated with compulsive obsessive disorder and drug addiction.

关键词： Optogenetics Adenosine A2A receptors dorsolateral striatum dorsomedial striatum habit goal-directed behavior

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Dynamic changes in hippocampal astrocytes in epileptic brain

Dynamic changes in hippocampal astrocytes in epileptic brain

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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： Preeti Joshi Department of Biophysics National Institute of Mental Health and Neurosciences

Neurons and astrocytes form an intimately connected network in the nervous system and there is compelling evidence demonstrating that neuronal networks alone are not sufficient for information processing, rather astrocytic network is also involved in physiological and pathological signaling in the nervous system. Epilepsy is characterized by synchronous hyperactivity of a group of neurons in the brain. The hyperactivity corresponds to the ictal discharges in electroencephalogram and peroxismal depolarization shifts in single cell recordings. In view of the neuron-astrocyte cross-talk it is imperative that astrocytes may play a role in pathogenesis of epilepsy. Purinergic signaling has emerged as an important mediator of neuron-glia signaling. Extracellular ATP modulates the synaptic activity through P2 Y receptors. We have studied the changes in purinergic receptor expression and function in an in-vivo model of temporal lobe epilepsy. It was observed that significant astrogliosis occurs in specific regions of hippocampus within 1-3 hr of status epilepticus(SE). In SE rats the expression of P2Y1 and P2Y2 receptors was drastically enhanced ascompared to control animals. Immunocytochemistry data revealed that the changes in P2Y1 and P2Y2 receptor expression are localized in astrocytes of stratum radiatum and stratum lacunosum moleculare regions. P2Y1 receptor agonist Me S-ADP inhibited the neuronal hyperactivity in SE rats. On the other hand activation of P2Y2 receptor using UTP appeared to enhance the neuronal hyperactivity. The astrocytic activity manifested as spontaneous Ca2+ oscillations was significantly enhanced in SE rats suggesting hyperactivity in astrocytes. Blockade of the spontaneous Ca2+ activity in astrocytes inhibited the spontaneous action potentials in the CA1 neurons in SE rats implying that the astrocytes certainly modulate the neuronal hyperactivity. Our results demonstrate that the functional characteristics of astrocytes alter at very early stage

关键词： Epilepsy,Neuron-astrocyte communication,P2Y receptors

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The synaptic connections between CSF-Contacting Nucleus and brainstem descending inhibitory system,and the effects of CSF-Contacting Nucleus lesion on nociceptive behaviors

The synaptic connections between CSF-Contacting Nucleus and ...

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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： Siyuan Song Licai Zhang Jiangsu Province Key Laboratory of Anesthesiology Xuzhou Medical College

CSF-Contacting Nucleus was firstly labeled and termed by our research group in brain. The neuronal somas of CSF-Contacting Nucleus locate in brain parenchyma, and their processes stretch into cerebrospinal fluid. Therefore, it can be inferred that CSF-Contacting Nucleus might play a pivotal role in modulating both neuro-neural and neuro-humoral circuits. Our previous studies suggested that the CSF-Contacting Nucleus might play a pivotal role in pain modulation. The crosstalk of CSF-Contacting Nucleus with other sites in the brain mediating the pain modulation remains unknown. The CSF-Contacting Nucleus locates in the brainstem. The brainstem descending inhibitory system(PAG, DR, RVM, and LC), a widely accepted sites in pain modulation, also locates in the brainstem. In the present study, we observed the synaptic connections between CSF-Contacting Nucleus and brainstem descending inhibitory system. Furthermore, we observed the effects of CSF-Contacting Nucleus lesion on rats' nociceptive behaviors. Thus, we could demonstrate morphological pathways and behavior proofs of CSF-Contacting Nucleus in pain modulation. Rats received BDA, an anterograde tracer, microinjections into the CSF-Contacting Nucleus. The morphological connections towards the brainstem descending inhibitory system(PAG, DR, RVM, and LC) were observed under light microscopy, and the synaptic connections were confirmed under electron microscopy. Also, PAG, DR, RVM and LC received BDA microinjections respectively. The morphologicalconnections towards the CSF-Contacting Nucleus were observed under light microscopy, and the synaptic connections were confirmed under electron microscopy. Furthermore, rats received CB-SAP microinjection into the lateral ventricle to damage CSF-Contacting Nucleus specifically. The number of residual neurons in the CSF-Contacting Nucleus, as well as rats' nociceptive behaviors(MWT and PWL) was evaluated at day 0, 1, 3, 5, 7, 10 after lesion. The correlation between the number o

关键词： CSF-Contacting Nucleus descending inhibitory system tract-tracing study synaptic connection target-lesion pain

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APP and its β-C-terminal fragment induce endosomal dysfunction and disrupt neurotrophic signaling

APP and its β-C-terminal fragment induce endosomal dysfunct...

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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： Wei Xu Xinyi Wang Fang Fang Liang Liang Chengbiao Wu Jianqing Ding Department of Neurology Shanghai Jiaotong University School of Medicine Ruijin Hospital Department of Neurosciences University of California Institute of Neurology Shanghai Jiaotong University School of Medicine Ruijin Hospital

Disruption of endosome-mediated signaling and trafficking of never growth factor(NGF) is believed to contribute prominently to atrophy and degeneration of basal forebrain cholinergic neurons(BFCNs) in Alzheimer's Disease(AD) and in Down syndrome(DS). However, the mechanism by which altered processing of amyloid precursor protein(APP) in AD or increased APP expression in DS leads to endosomal dysfunctions remains unclear. We first confirmed that Rab5-positive early endosomes were increased both in numbers and sizes in cultures of BFCNs in Ts65 Dn, a mouse model of DS. To further dissect the molecular and cellular pathways by which Rab5 function was dysregulated by excessive APP or its C-terminal fragments(CTFs), we examined the effect of various APP constructs on the activity of Rab5- and the size of early endosomes. Our results show that early endosomes were abnormally enlarged in both PC12 cells and primary BFCNs by either expressing the full length wild type APP, or an APP Swedish mutant, or the β-CTF. In addition, the GTP-bound form i.e. the activated form, of endogenous Rab5 was increased under these conditions. When stimulated with NGF, the differentiation of PC12 cells was impaired in these cells. Interestingly, the inhibitory effect can be partially ameliorated reduced by the Rab5S34 N dominant negative Rab5 mutant. Taken together, our results provide strong evidence that excessive APP/β-CTF is linked to abnormal activation of Rab5 that impairs NGF signaling and trafficking, resulting in atrophy and degeneration of BFCNs.

关键词： APP/β-CTF early endosome Rab5 Alzheimer's disease NGF signaling Basal forebrain cholinergic neurons(BFCNs)

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Brain-derived neurotrophic factor protects large retinal ganglion cells following acute optic nerve crush injury

Brain-derived neurotrophic factor protects large retinal gan...

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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： Zhen Puyang Liang Feng Hui Chen Peiji Liang John B.Troy Xiaorong Liu School of Biomedical Engineering Shanghai Jiao Tong University Department of Ophthalmology Feinberg School of MedicineNorthwestern University Department of Biomedical Engineering Robert R.Mc Cormick School of Engineering and Applied ScienceNorthwestern University Department of Neurobiology Weinberg College of Arts and SciencesNorthwestern University

Objective Brain derived neurotrophic factor（BDNF） is known to regulate neuronal differentiation and survival in the central nervous system. For a number of neurodegenerative and psychiatric disorders, BDNF has been shown to play an important role in both their pathogenesis and treatment. Here we investigated whether BDNF preserved retinal ganglion cells（RGCs） against the acute optic nerve crush injury. Methods Using a tamoxifen-induced Cre system, BDNF was over-expressed in the mouse retina. We performed the partial optic nerve crush（p ONC） to induce RGC degeneration. The survival of Thy-1-YFP positive RGCs was monitored with the Micron III in vivo imaging system and RGC somas were counted using a customized Matlab program. In vitro confocal images were taken at different time points post p ONC for axon counting. Results（1） Retinal BDNF was up-regulated in the BDNF overexpression（BDNFE） mice.（2） Large Thy-1-YFP positive RGC somas were identified in the in vivo retinal images, which was confirmed by double-immunostaining with RGC markers.（3） A significant RGC loss was found in control group following the p ONC. By contrast, more RGCs survived in BDNFE mice.（4） The axon loss is also significantly reduced in the BDNFE mice at 2 weeks post p ONC injury. Conclusion Our results demonstrated that the over-expression of BDNF delayed the RGC and axon loss following the partial optic nerve crush injury. Our studies provide new insights on how BDNF protects RGCs and preserve vision against the optic nerve injury.

关键词： BDNF optic nerve crush injury in vivo retinal imaging

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