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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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Clk1 participates in neuroglial activation and neurotoxicity in MPTP mouse model of Parkinson's disease

Clk1 participates in neuroglial activation and neurotoxicity...

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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： Ruinan GU Fali ZHANG Longtai ZHENG Xuechu ZHEN Department of Pharmacology College of Pharmaceutical SciencesSoochow University

The present study is designed to investigate the roles of clk1 gene in dopaminergic neuron activity an its potential implication in Parkinson's disease(PD). METHODS Subchronic MPTP mouse model(MPTP, 30mg/kg, 5 days) was employed in male Mclk1+/- mutant *** tests were performed 7 days after MPTP treatment, immunological histochemistry(IHC) was carried on after behavioral tests. Primary astrocyte of WT andMclk1+/- mutant was used to investigate the role of clk1 in inflammatory response. The expression of inflammatory cytokines and proinflammatory factors were assessed by real-time PCR, ELISA and NO assay. The role of clk1 in the intracellular level of reactive oxygen species(ROS) generation and mitochondrial membrane potential were also investigated by using fluorescent probe DCFH-DA and JC-1, respectively. RESULTS In response to MPTP treatment, Mclk1+/- mutant mice showed more severe DA neuron loss and severe motor coordination impairment. We also detected and increased reactive glial response as compared with wild-type mice Primary cultured glial cells from Mclk1+/- mice exhibited significant high proinflammatory cytokines, higher intracellular ROS and lower mitochondrial membrane potential in response to LPS/IFN-γtreatment. Moreover, conditioned media from clk1 depleted glial cells promoted death of cultured DA neurons. We further provided evidence showing that Clk1 elicits the effects via HIF-1α. CONCLUSION These findings provided the first evidence that Mclk+/- is involved in DA neuronal regulation via modulating neuroglial inflammatory response.

关键词： Parkinson's disease(PD) glial cells clk1

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Aged monkey brains reveal the role of ubiquitin-conjugating enzyme UBE2N in the synaptosomal accumulation of mutant huntingtin

Aged monkey brains reveal the role of ubiquitin-conjugating ...

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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： Peng Yin Zhuchi Tu An Yin Sen Yan Xiangyu Guo Junxia Zhou Shihua Li Xiao-Jiang Li State Key Laboratory of Molecular Developmental Biology Institute of Genetics and Developmental BiologyChinese Academy of Sciences Department of Human Genetics Emory University School of Medicine

Misfolded proteins are ubiquitinated and cleared by the proteasome, they can accumulate in synapses in aged neurons to promote synaptic dysfunction in a variety of neurodegenerative diseases, including Huntington's disease, which is caused by polyglutamine expansion in huntingtin. The mechanism behind this aging-related phenomenon is unknown and has been difficult to investigate using animals with short life spans. With brain tissues from longer-lived rhesus monkeys of different ages, we found that aging reduces ubiquitin-proteasomal activity and also increases the level of ubiquitin-conjugating enzyme UBE2 N in synaptosomes. Synaptosomal fractions from aged monkey brain increase in vitro ubiquitinated huntingtin, whereas depletion of UBE2 N markedly reduces this increase. Overexpressing UBE2 N increases the aggregation of mutant huntingtin, and reducing UBE2 N attenuates huntingtin aggregation in cellular and mouse models of HD. Thus, age-dependent decrease of the UPS activity may lead more mutant huntingtin to be ubiquitinated via UBE2 N in the synaptosomes. The K63-mediated ubiquitination will contribute to the accumulation of mutant huntingtin in the synaptosomes in aged brain and related neuropathology. The reducing UBE2 N in aged neurons could help decrease synaptic accumulation of mutant huntingtin and perhaps other misfolded proteins, as well. Our studies suggest that increased UBE2 N plays a critical role in the synaptosomal accumulation of mutant protein associated with age and neurodegeneration disease.

关键词： ubiquitin-conjugating enzyme Huntington's disease protein accumulation aging

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Endogenous orexinergic system modulates the firing activity of pallidal neurons in vivo

Endogenous orexinergic system modulates the firing activity ...

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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： Yu-Ting Yang Yan Xue Hong-Xia Liu Xiu-Ping Shang Lei Chen Department of Physiology Qingdao University

Orexin is a member of neuropeptides family which was first identified in the hypothalamus. Much evidence has shown that central orexinergic systems are closely related to Parkinson's disease. The globus pallidus receives orexinergic innervation arising from the hypothalamus. Morphological studies have shown the expression of both orexin-1 and orexin-2 receptors in the globus pallidus. However, up to present, the in vivo electrophysiological and behavioral consequences of endogenous orexinergic system in the globus pallidus are unknown. In this study, we elucidated the in vivo effects of endogenous orexinergic system on the firing activity of globus pallidus neurons in rats. Micro-pressure administration of 0.1μM SB-334867, the specific OX1 receptor antagonist, significantly decreased the spontaneous firing rate of pallidal neurons in 25 pallidal neurons recorded(basal: 15.98±2.67 Hz;SB-334867: 11.91±2.18 Hz;P<0.001). The average decrease was 32.80±3.84%, which was significantly decreased(P<0.001) compared to that of vehicle(normal saline) group(The average increase was 3.28±1.43%).(2) Next, micropressure ejection of 0.1m M, 0.01 m M, 0.1μM, 1n M and 0.01 n M SB334867 decreased the basal spontaneous firing rate by 17.62±3.20%, 23.53±4.69%, 32.80±3.84%, 25.20±5.74% and 18.11±3.92%, respectively. A negative correlation between SB334867-induced change in firing rate and basal firing level were observed in the globus pallidus neurons(P<0.01). The present results suggested that endogenous orexin-1 receptors are involved in the modulation of firing activity of globus pallidus neurons.

关键词： Orexin SB-334867 globus pallidus single unit recording

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GABAergic inputs at the axon initial segment yield timing-dependent bidirectional effects in the integration with dendritic excitatory inputs

GABAergic inputs at the axon initial segment yield timing-de...

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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： Nan Liu Xiaohui Zhang State Key Laboratory of Cognitive Neuroscience and Learning IDG/McGovern Institute for Brain ResearchBeijing Normal University

GABAergic synaptic inputs derived from chandelier cells locate exclusively at the axon initial segment(AIS) of pyramidal cells(PCs). Experimental evidences showed that these GABAergic inputs elicit depolarizing membrane potential changes from resting state, and induce both excitatory and inhibitory impacts on the activity of postsynaptic PCs with an dependence of the ongoing membrane potential levels. However, the integration of GABAergic synaptic inputs at the AIS with dendritic excitatory inputs remains quantitatively elusive. Here by performing realistic NEURON modeling of a layer 5 cortical PC, we show that the depolarizing GABAergic input at the AIS could exert both facilitation and suppression effects in the summation with the dendritic excitatory synaptic inputs. Our results indicates that there exist two nonlinear components, the boosting effect and the shunting effect, which are attributed to the activation of the enriched voltage-gated Nav1.6 channels and GABAA receptors at the AIS, respectively. These two components results in timing-dependent super-linear and sub-linear integration when the GABAergic input at the AIS summate asynchronously with dendritic excitatory synaptic inputs. We further showedthat such timing-dependent nonlinear integration at the AIS bi-directionally modulate the probability and timing reliability of the neuronal spike generation in PCs. These modeling results are now being verified in the electrophysiological recording from neocortical layer 5 PCs in acute brain slices. Thus, our quantitative modeling reveals a biophysical mechanism by which the depolarizing GABAergic inputs at AIS, originated from the chandelier cells, exert the non-linear and bi-directional impact on the integration of subthreshold inputs and the generation of neuronal spikes in a neocortical PC.

关键词： chandelier cell GABA excitation shunting inhibition nonlinear integration axonal initial segment

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Erasure of recent and remote hippocampus-dependent fear memory by enhancing memory forgetting through increase in adult hippocampal neurogenesis

Erasure of recent and remote hippocampus-dependent fear memo...

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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： Satoshi KIDA Department of Bioscience Tokyo University of Agriculture

Erasure of fear memory is thought to be a therapeutic target for emotional disorders such as post-traumatic stress disorders. Memantine(MEM) is an N-methyl-D-aspartate glutamate receptor antagonist. Previous studies showed that MEM induced enhancement of adult hippocampal neurogenesis and memory forgetting formed recently. In this study, we tried to examine the effects of MEM treatment on forgetting of fear memory. Mice were contextual fear-conditioned with an electrical footshock(training) and then received systemic injections of MEM(50 mg/kg) once a week for 4 weeks. We found that MEM group displayed forgetting of contextual fear memory following the MEM treatment, while control group treated with VEH displayed normal contextual fear memory. Importantly, MEM group did not show spontaneous recovery of fear memory even a month after the MEM treatment. We next examined the relationship between forgetting of fear memory and increase in adult neurogenesis by MEM. After training, mice received injections of MEM followed by injections of 5-bromo-2-deoxyuridine(Brd U;50 mg/kg) 2 days later. Interestingly, there was a significant negative correlation between the number of Brd U-positive cells increased by MEM and differences of freezing scores before and after the MEM treatment. Moreover, MEM group displayed forgetting of hippocampus-dependent inhibitory avoidance memory, but not amygdala-dependent cued fear memory. These observations suggest that MEM treatment enables to erase hippocampus-dependent fear memory by enhancing memory forgetting through the increase in adult hippocampal neurogenesis. We are now examining effects of the MEM treatment on remote fear memory.

关键词： MEM Erasure of recent and remote hippocampus-dependent fear memory by enhancing memory forgetting through increase in adult hippocampal neurogenesis

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Autocrine action of BDNF on dendrite development of adult-born hippocampal neurons

Autocrine action of BDNF on dendrite development of adult-bo...

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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 Wang Xingya Chang Liang She Duo Xu Wei Huang Mu-ming Poo Institute of Neuroscience State Key Laboratory of Neuroscience and CAS Center for Excellence in Brain ScienceShanghai Institutes for Biological SciencesUniversity of Chinese Academy of Sciences

Dendrite development of newborn granule cells(GCs) in the dentate gyrus of adult hippocampus is critical for their incorporation into existing hippocampal circuits, but the cellular mechanisms regulating their dendrite development remains largely unclear. In this study, we examined the function of brain-derived neurotrophic factor(BDNF), which is expressed in adult-born GCs, in regulating their dendrite morphogenesis. Using retrovirus-mediated gene transfection, we found that deletion and overexpression of BDNF in adult-born GCs resulted in the reduction and elevation of dendrite growth, respectively. This effect was mainly due to the autocrine rather than paracrine action of BDNF, because deletion of BDNF only in the newborn GCs resulted in dendrite abnormality of these neurons to a similar extent as that observed in conditional knockout(c KO) mice with BDNF deleted in the entire forebrain. Furthermore, selective expression of BDNF in adult-born GCs in BDNF c KO mice fully restored normal dendrite development. The BDNF autocrine action was also required for the development of normal density of spines and normal percentage of spines containing the postsynaptic marker PSD-95, suggesting autocrine BDNF regulation of synaptogenesis. Furthermore, increased dendrite growth of adult-born GCs caused by voluntary exercise was abolished by BDNF deletion specifically in these neurons, and elevated dendrite growth due to BDNF overexpression in these neurons was prevented by reducing neuronal activity with co-expression of inward rectifier potassium channels, consistent with activity-dependent autocrine BDNF secretion. Thus, BDNF expressed in adult-born GCs plays a critical role in dendrite development by acting as an autocrine factor.

关键词： Autocrine action of BDNF on dendrite development of adult-born hippocampal neurons

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Study on the effect of Neuropeptide (Nesfatin-1) on epileptic discharges in rat insular cortex neurons

Study on the effect of Neuropeptide (Nesfatin-1) on epilepti...

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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： Shuang-lai Ren Zheng Liu Tao Sun NingXia key Laboratory of Cerebrocranial Disease Ningxia Medical University NingXia Institute of Medical Sciences Depatment of Neurosurgery Affiliated Hospital of Ningxia Medical University

Nesfatin-1 is the discovered peptide hormones involved in the control of appetite in 2006. Besides its main appetite-control function, it causes depolarization in the paraventricular nucleus(PVN). However, the effect of nesfatin-1 on epilepsy is still not clear. Our research found that serum and hypothalamus nesfatin-1 levels from epilepsy rat kindled by kainic acid was significantly higher(P<0.05)than control group rat's level. The expression of Nesfatin-1 was decreased significant(P<0.05)after anti-epilepsy with valproate(VPA) treatment, while higher than the blank control group. Tissue samples were analyzed for nesfatin-1 expression by immunochemistry, serum nesfatin-1 levels by ELISA. Epilepsy is one of the most common neurological disorders. In order to further investigate the antiepileptic mechanism of nesfatin-1, the patch clamp technique is used to observe the effects of nesfatin-1 on 4-aminopyridine(4-AP) induced epileptiform events in neurons of rat insular slices. We used voltage clamp-whole cell recording mode to acquire electric currents by Gap Free protocol, 10μM nesfatin-1 was added through ACSF perfusion in brain slices for more than 20 minutes, we found no significant change of epileptiform induced by 4-AP(n=6), such as, the generation frequency of epilepsy, and generation mode of epilepsy. So the exactitude detection of expression level of Nesfatin-1 in the serum could reflect the neuropeptide variance level in hypothalamus. This method could be the simpler, sensitive and noninvasive way on epilepsy diagnose, but is not good potent target for epilepsy therapy.

关键词： epilepsy Nesfatin-1 insular cortex brain slices patch clamp

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Selective activation of cholinergic basal forebrain neurons induces immediate sleep-wake transitions

Selective activation of cholinergic basal forebrain neurons ...

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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： Yong Han Yu-feng Shi Wang Xi Rui Zhou Zhi-bing Tan Hao Wang Xiao-ming Li Zhong Chen Guoping Feng Minmin Luo Zhi-li Huang Shumin Duan Yan-qin Yu Department of Neurobiology Key Laboratory of Medical Neurobiology of Ministry of Health of ChinaKey Laboratory of NeurobiologyZhejiang University School of Medicine Department of Neurobiology Duke University Medical Center National Institute of Biological Sciences Department of Pharmacology Shanghai Medical CollegeFudan University

The basal forebrain(BF) plays a crucial role in cortical activation. However, the exact role of cholinergic BF neurons in the sleep-wake cycle remains unclear. Wedemonstrated that photostimulation of cholinergic BF neurons genetically targeted with channelrhodopsin 2(Ch R2) was sufficient to induce an immediate transition to waking or rapid eye movement(REM) sleep from slow-wave sleep(SWS). Light stimulation was most likely to induce behavioral arousal during SWS, but not during REM sleep, a result in contrast to the previously reported photostimulation of noradrenergic or hypocretin neurons that induces wake transitions from both SWS and REM sleep. Furthermore, the ratio of light-induced transitions from SWS to wakefulness or to REM sleep did not significantly differ from that of natural transitions, suggesting that activation of cholinergic BF neurons facilitates the transition from SWS but does not change the direction of the transition. Excitation of cholinergic BF neurons during wakefulness or REM sleep sustained the cortical activation. Stimulation of these neurons for 1 hr induced a delayed increase in the duration of wakefulness in the subsequent inactive period. Our results suggest that activation of cholinergic BF neurons alone is sufficient to suppress SWS and promote wakefulness and REM sleep.

关键词： Basal forebrain,Cholinergic neurons,Optogenetics,Sleep-wake modulation

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Sleep Deprivation and Cognitive Impairments in Female Rats:The Beneficial Effects of Exercise

Sleep Deprivation and Cognitive Impairments in Female Rats:T...

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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： Vahid Sheibani Hakimeh Saadati Mohammad reza Afarinesh Neuroscience Research Center Institute of NeuropharmacologyKerman University of Medical Sciences

Inadequate sleep is a common problem in modern societies. Physical exercise has been suggested to attenuate the cognitive impairments induced by sleep deprivation(SD) in male rats. Female rats are more vulnerable to the deleterious effects of SD on cognitive functions. The objective of the current study was to investigate the effects of physical exercise on learning and memory, LTP and the levels of BDNF m RNA and protein in the hippocampus of female rats following SD. Intact and ovariectomiezed(OVX) female Wistar rats were used in the present study. The exercise protocol was four weeks treadmill running and the multiple platform method was applied to induce 72 h SD. The cognitive functions were evaluated by using Morris water maze(MWM) and field potential recording in the CA1 area of the hippocampus. Quantitative RT-PCR and immunoblot analysis were used to evaluate the level of hippocampus BDNF m RNA and protein, respectively. Learning and short term memory of sleep-deprived OVX rats were impaired compared to the intact and the OVX groups in MWM(p< 0.05). Field potential recording data indicated that the induction and maintenance phase of E-LTP impaired in the sleep deprived animals compared to the other groups. Physical exercise alleviated the SD-induced behavioral performances and E-LTP impairments in both intact and OVX groups(p<0.05). Also, protein and m RNA expression of BDNF was significantly(p<0.05) decreased after SD in OVX rats in compared with other groups. Furthermore, sleep deprived OVX rats under exercise conditions had a significant(p< 0.05) up-regulation of the m RNA and BDNF protein. In conclusion, the regular exercise can improve the cognitive functions deficits in sleep-deprived female rats and exert a protective effect against hippocampus-related impairments induced by SD probably by inducing BDNF expression.

关键词： Exercise,sleep deprivation,learning and memory,LTP and BDNF

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IL-2 inhibits the differentiation of mice CD4+CD62L+T cells into Th17 and promotes the differentiation of Treg

IL-2 inhibits the differentiation of mice CD4+CD62L+T cells ...

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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： Jun Zhou Ting Wang Rui-Qin Yao Xue-Bin Qu Dept.of Cell Biology & Neurobiology Xuzhou Medical College

The study is to investigate the effect of IL-2 on the differentiation of mice spleen CD4+CD62L+T cells into Th17 in vitro. CD4+CD62L+T cells from C57BL/6 mice with MACS were divided into two groups, control group and IL-2 treated group. Cell proliferation, cell apoptosis, the concentration of cytokine IL-17 A, IL-23,IL-6, TGF-β, IL-10, IL-35, expression level of specific transcription fator Rorγt, and percentage of CD4+IL-17+Th17 and CD4+Foxp3+Treg were measured by CFSE fluorescent staining, Annexin V-PI, ELISA, qR T-PCR, and FACS, respectively. Compared with control group, the proliferation was improved(P<0.05) with a reducing apoptosis(P<0.05) in IL-2 treated cells. Moreover, IL-2 treated cells produced significantly lower concentration of IL-17 A, IL-23, IL-6 and higher concentration of TGF-β, IL-10, IL-35(P<0.05). Besides, the percentage of CD4+IL17+Th17 were reduced(P<0.05) and CD4+Foxp3+Treg were increased(P<0.05) compared with control group. IL-2 treated cells also produced lower expression level of Rorγt(P<0.05) and higher expression level of Foxp3(P<0.05) compared with control group. The results indicated that IL-2 could facilitate T cell proliferation, promote the differentiation of Treg and inhibit the differentiation of Th17.

关键词： interleukin-2 helper T cell 17 proliferation differentiation

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