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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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Electrophysiological and behavioral effects of angiotensin Ⅱ on pallidal neurons in normal rats

Electrophysiological and behavioral effects of angiotensin ...

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

The globus pallidus plays a critical role in movement regulation. More recent studies suggested the brain RAS exerted a major role in dopaminergic neuron degeneration of Parkinson's disease. Previous studies revealed the expression of angiotensin Ⅱm RNA in the globus pallidus. However, little is known about the functions of angiotensin Ⅱ in the globus pallidus. In the present studies, in vivo and in vitro electrophysiological recordings, as well as behavioral test were used to investigate the effects of angiotensin Ⅱ in the globus pallidus. In normal rats, micro-pressure ejection of angiotensin Ⅱ increased the frequency of spontaneous firing in a dose-dependent manner. Angiotensin Ⅱ at 10μM increased the frequency of spontaneous firing from 16.4±3.1 Hz to 23.4±4.5 Hz in 14 out of the 20 pallidal neurons. The average increase in firing rate was 44.7±8.7%, which was significantly increased(P<0.001) compared to that of vehicle group. Angiotensin Ⅱ did not change the firing pattern significantly. Consistent with the in vivo studies, preliminary results showed that when the cells were voltage clamped at-70 mV, angiotensin Ⅱ induced a small inward current in the presence of 0.5μM TTX. Furthermore, angiotensin Ⅱ increased the frequency of miniature inhibitory postsynaptic currents(m IPSCs) in some pallidal neurons. Finally, behavioral studies revealed that angiotensin Ⅱ(10μM) alleviated the symptoms of rigidity caused by haloperidol. Losartan, the blocker of angiotensin Ⅱ type 1 receptor, blocked both the electrophysiological and behavioral effects induced by angiotensin Ⅱ. The present results suggested that activation of pallidal angiotensin Ⅱ type 1 receptor may be involved in angiotensin Ⅱ-induced antiparkinsonian effects by increasing the activity of pallidal neurons.

关键词： globus pallidus angiotensin Ⅱ spontaneous firing

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In vivo conversion of dorsal midbrain astrocytes into functional neurons

In vivo conversion of dorsal midbrain astrocytes into functi...

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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： Yueguang Liu Qinglong Miao Jiacheng Yuan Su'e Han Panpan Zhang Sanlan Li Zhiping Rao Wenlong Zhao Qian Ye Junlan Geng Xiaohui Zhang Leping Cheng Institute of Neuroscience and State Key Laboratory of Neuroscience Shanghai Institutes for Biological SciencesChinese Academy of Sciences State Key Laboratory of Cognitive Neuroscience and Learning & IDG/McGovern Institute for Brain Research Beijing Normal University University of Chinese Academy of Sciences

Studies of induced pluripotent stem cells(iP SCs) and more recent findings that defined transcription factors can directly convert fibroblasts to functional neurons demonstrate the feasibility of transdifferentiation of non-neuronal cells directly into neurons. In vivo induction of non-neuronal cells into neurons by transcription factors offers potential therapeutic approaches for neural regeneration. Although generation of induced neuronal(iN) cells in vitro and in vivo has been reported, whether iN cells can be fully integrated into existing circuits remains unclear. Here we show that expression of achaete-scute complex homolog-like 1(Ascl1) alone is sufficient to convert dorsal midbrain astrocytes of mice into functional i N cells in vitro and in vivo. Specific expression of Ascl1 in astrocytes by infection with GFAP-AAV vector converts astrocytes in dorsal midbrain, striatum, and somatosensory cortex of postnatal and adult mice into functional neurons in vivo. These iN cells mature progressively, exhibiting neuronal morphology and markers, action potentials, and synaptic inputs from and output to existing neurons. Both glutamatergic and GABAergic neurons exist in the Ascl1-inducd iN cells. Thus, a single transcription factor Ascl1 is sufficient to convert brain astrocytes into functional neurons, and GFAP-AAV is an efficient vector for generating iN cells from astrocytes in vivo.

关键词： astrocyte-to-neuron conversion induced neuronal(iN) cells proneural gene Ascl1 transdifferentiation

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Possible contribution of K+-Cl- cotransporter 2 down-regulation in the ventral posterior nucleus of the thalamus in rats with neuropathic pain

Possible contribution of K+-Cl- cotransporter 2 down-regulat...

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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： Meng Zhang Yu Zhang Lu-Peng Yue Jun Ma Wen Chen Feng-Yu Liu Ming Yi You Wan Neuroscience Research Institute Peking University Key Laboratory for Neuroscience Ministry of Education/ National Health and Family Planning CommissionPeking University Department of Neurobiology School of Basic MedicinePeking University

Neuropathic pain is difficult to treat in clinic because of insufficient understandings of its mechanisms. Except for peripheral sensitization from injury and inflammation, central sensitization plays an important role. The ventral posterior(VP) nucleus of the thalamus is the main gate where somatosensory information enters the brain. One of the mechanisms of central sensitization in neuropathic pain is dis-inhibition of GABAergic and glycinergic activities. In adults, inhibitory effects of g-aminobutyric acid receptor subtype A(GABAA) and glycine receptors depend on the low intracellular chloride(Cl-) concentration, which is maintained by the potassium-chloride cotranspoter KCC2. In the present study, we examined the change of KCC2 expression in the VP nucleus in neuropathic pain rats and provided preliminary evidence for its possible role. In a neuropathic pain model of rats with spared nerve injury(SNI), a significant down-regulation of KCC2 was observed first in the contralateral VP nucleus, then in the ipsilateral. After injection of furosemide, a KCC2 blocker, in the VP nucleus in na?ve rat, mechanical allodynia developed. Considering the abundant evidence from previous reports that the decreased KCC2 leads to a dis-inhibition of postsynaptic GABAergic / glycinergic activities and thus increases the excitability of the neuron, our results suggest that the decreased expression of KCC2 in the VP nucleus may increase the neuron hyperexcitability and thus contribute to neuropathic pain.

关键词： KCC2 neuropathic pain spared nerve injury mirror pain furosemide GABA

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A Mechanism for Graded,Dynamically Routable Current Propagation in Pulse-Gated Feedforward Neuronal Networks

A Mechanism for Graded,Dynamically Routable Current Propagat...

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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： Andrew T.Sornborger Zhuo Wang Louis Tao Department of Mathematics University of California at Davis Center for Bioinformatics College of Life SciencesPeking University

Neural oscillations can enhance feature recognition, modulate interactions between neurons, and improve learning and memory. Numerical studies have shown that coherent spiking can give rise to windows in time during which information transfer can be enhanced in neuronal networks. Unanswered questions are: 1) What is the transfer mechanism? And 2) how well can a transfer be executed? Here, we present a pulse-based mechanism by which a graded synaptic current amplitude may be exactly propagated from one neuronal population to another. The mechanism relies on the downstream gating of mean synaptic current amplitude from one population of neurons to another via a pulse. Because transfer is pulse-based, information may be dynamically routed through a neural circuit with fixed connectivity. We demonstrate the transfer mechanism in a realistic network of spiking neurons and show that it is robust to noise in the form of pulse timing inaccuracies, random synaptic strengths and finite size effects. We also show that the mechanism is structurally robust in that it may be implemented using biologically realistic pulses. The transfer mechanism may be used as a building block for fast, complex information processing in neural circuits. We show that the mechanism naturally leads to a framework wherein neural information coding and processing can be considered as a product of linear maps under the active control of a pulse generator. Distinct control and processing components combine to form the basis for the binding, propagation, and processing of dynamically routed information within neural pathways. Using our framework, we construct example neural circuits to 1) maintain a short-term memory, 2) compute time-windowed Fourier transforms, and 3) perform spatial rotations. We postulate that such circuits, with automatic and stereotyped control and processing of information, are the neural correlates of Crick and Koch's zombie modes.

关键词： coding,coherence,synfire chains

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JNK-mediated activation of ATF2 contributes to dopaminergic neurodegeneration in the MPTP mouse model of Parkinson's disease

JNK-mediated activation of ATF2 contributes to dopaminergic ...

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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： Qiaoying Huang Xiaoxiao Du Xin He Qing Yu Kunhua Hu Wolfgang Breitwieser Shanshan Ma Mingtao Li Department of Pharmacology Zhongshan School of MedicineSun Yat-sen University Guangdong Province Key Laboratory of Brain Function and Disease Zhongshan School of MedicineSun Yat-sen University

The JNK/c-Jun pathway is a known critical regulator of dopaminergic neuronal death in Parkinson's disease(PD) and is considered a potential target for neuroprotective therapy. However, whether JNK is activated within dopaminergic neurons remains controversial, and whether JNK acts through downstream effectors other than c-Jun to promote dopaminergic neuron death remains unclear. In this study, we confirm that JNK but not p38is activated in dopaminergic neurons after MPTP-intoxication. Furthermore, within the dopaminergic neurons of the substantia nigra in MPTP-treated mice, JNK2/3 selectively phosphorylates threonine 69(Thr69) of ATF2, a transcription factor of the ATF/CREB family, whereas the phosphorylation of Thr71 is constitutive and remains unchanged. The increased phosphorylation of ATF2 on Thr69 by JNK in the MPTP mouse model suggests a functional relationship between the transcriptional activation of ATF2 and dopaminergic neuron death. By using dopaminergic neuron-specific conditional ATF2 mutant mice, we found that either partial or complete deletion of the ATF2 DNA-binding domain(ATF2-DBD) in dopaminergic neurons markedly alleviates the MPTP-induced dopaminergic neurodegeneration, indicating that the activation of ATF2 plays a detrimental role in neuropathogenesis in PD. Taken together, our findings demonstrate that JNK-mediated ATF2 activation contributes to dopaminergic neuron death in an MPTP model of PD.

关键词： Parkinson's disease dopaminergic neurodegeneration JNK ATF2

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PICK1 Deficiency Impairs Glutathione Synthesis and Increases Oxidative Stress via Reduction of Surface EAAC1

PICK1 Deficiency Impairs Glutathione Synthesis and Increases...

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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： Ya-Nan Wang Liang Zhou Zhen Wang Ying-Cong Li Ya-Wen Zhang Ying Shen Department of Neurobiology Key Laboratory of Medical Neurobiology of the Ministry of HealthZhejiang Province Key Laboratory of NeurobiologyZhejiang University School of Medicine

Protein interacting with C-kinase 1(PICK1) has received considerable attention, as it interacts with a broad range of neurotransmitter receptors, transporters and enzymes, and thereby influences their localization and function in the central nervous system. Although it is suggested that putative partners of PICK1 are involved in neurological diseases such as schizophrenia, Parkinson's disease, chronic pain, and amyotrophic lateral sclerosis, the functions of PICK1 in neurological disorders are not clear. Here, we show thatoxidative stress, which is tightly associated with neurological diseases, occurs in PICK1-/-mice. The oxidation in PICK1-/- mice was found selectively in neurons and was age-dependent, leading to microglial activation and the release of inflammatory factors. Neurons in the cortex and hippocampus from PICK1-/- mice showed increased vulnerability to oxidants and reduced capacity to metabolize reactive oxygen species;this was caused by reduced glutathione content and impaired cysteine transport. The dysregulated expression of glutathione was attributed to a decrease of the surface glutamate transporter EAAC1. Overexpression of PICK1 could rescue the surface expression of EAAC1 and ameliorate the glutathione deficit in PICK1-/- neurons. Finally, reduced surface EAAC1 was associated with defective Rab11 activity. Transfection with dominant negative Rab11 effectively suppressed surface EAAC1 and increased ROS production. Taken together, these results indicate that PICK1 is a crucial regulator in glutathione homeostasis and may play important roles in oxidative stress and its associated neurodegenerative diseases.

关键词： PICK1 oxidative stress EAAC1 glutathione Rab11 oxidant

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Effects of zeatin on depression-like behaviors in rats with chronic unpredictable stress

Effects of zeatin on depression-like behaviors in rats with ...

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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： Ting-Ting CAI Jun-YAO Wei-Wei GE Yu-Ting TANG Hong-Ping HUANG Meng-Ya WANG Cell Electrophysiology Laboratory Wannan Medical College Rising-Star Group Wannan Medical College

Objective To explore the effects of zeatin on depression-like behaviors in rats with chronic unpredictable stress. Methods Thirty-four male SD rats were randomly divided into 3 groups, model group(n=12), model+zeatin group(n=12), and normal+zeatin group(n=10). To prepare depressive-like behavior model animal, rats in model and model+zeatin groups were treated by using chronic unpredictable stress stimulation and solitary feeding for 21 days. After the testing of open-field and sugar consumption, rats in model+zeatin and normal+zeatin groups were intraperitoneally injected with zeatin(10mg/kg, qd) for 9 days, while rats in model group were administered with same volume of normal saline. On the 9th day of treatment, the open-field test and sugar consumption test were carried out again. Results The data of open-field test and sugar consumption test prior to zeatin treatment showed that depressive-like behavior model rats were successfully established. After 9 days of zeatin treatment, the open field test scores and sugar consumption were significantly different among 3 groups(P<0.05), and those in model+zeatin group were both increased as compared with decrease in normal+zeatin group(P<0.05). Conclusion The preliminary results suggest that zeatin may have distinct effects on depression-like behavior model rats with chronic unpredictable stress and on normal rats.

关键词： zeatin depression chronic unpredictable stress

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PINK1 and Parkin crosstalk synucleinopathies by mitophagy

PINK1 and Parkin crosstalk synucleinopathies by mitophagy

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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： Jian-She Wei Ping Li Yi Wang Jian-Nan Wu Nan-Nan Wei Zhi-Quan Zhao Wen-Jin Xia Cong-Cong Li Institute for Brain Science Research Laboratory of Brain Function and Molecular NeurodegenerationSchool of Life SciencesHenan University Institute for Brain Science Research Laboratory of Neural Optogenetics InnovationSchool of Life SciencesHenan University

PINK1 is a mitochondrial serine/threonine kinase, which protects mitochondria from cellular stress and regulates neuronal differentiation. Mutations in PINK1 and Parkin, a ubiquitin ligase, cause early-onset familial Parkinson's disease(AR-JP) respectively. There are many reports for the functions of PINK1/parkin at home and abroad, but the precise mechanism of PINK1/parkin in Parkinson's disease remains unknown. This project will explore the protective effect of PINK1/Parkin on mitophagy, and investigate the role of PINK1/Parkin on β-syn P123 H autophagic degradation. We construct the Parkin plasmid in Tet-off system and establish the stable Parkin over-expressing cell lines. We observe Parkin cellular distribution and function by immunofluorescence and immunoblot *** cell viability and degeneration is analyzed by LDH, WST-1 and TUNEL assays. PINK1 mutations induce mitochondrial rupture and aggregation, and result in cell activity reduction and toxicity. Parkin mutants aggregate in cells and lead to reduction of mitochondrial membrane potential. Wild-type PINK1 and Parkin are involved in mitochondrial quality control, and they can promote the β-syn P123 H autophagic degradation. Mitochondrial autophagy and fission/fusion are mediated by mitochondrial-associated protein PINK1/Parkin, and they play the protective roles in Synucleinopathies induced by β-syn P123 H associated with dementia with Lewy bodies.

关键词： PINK1 Parkin Mitophagy Fission Fussion Synucleinopathies

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Low intensity treadmill exercise enhances synaptic plasticity and CREB phosphorylation in the hippocampus of rats

Low intensity treadmill exercise enhances synaptic plasticit...

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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： Sun Li-na Li Hai-chun Zhang Xin-xin Qi Jin-shun Department of Physiology Key Laboratory for Cellular Physiology of Ministry of EducationShanxi Medical University School of PE Taiyuan University of Technology

Objective: To investigate the effects of low intensity treadmill exercise on cognitive behavior of rats and its underlying electrophysiological and signal transduction mechanisms. Methods: Male Wistar rats were randomly divided into control group(CG) and exercise group(EG). The rats in EG were trained for 8 weeks on the treadmill with low intensity(8 m/min;30 min/d), while the rats in CG was not intervened. After training, Y-maze spontaneous alternation and active avoidance experiments were performed. Then, the in vivo late phase long-term potentiation(L-LTP) of hippocampal field excitatory postsynaptic potentials(f EPSPs) was recorded. After sacrifice, the level of phosphorylated c AMP response element-binding protein(P-CREB), in hippocampus was tested using western blotting. Results:(1) Low intensity exercise significantly enhanced the learning and memory ability of rats in Y-maze tests(P<0.05).(2) Low intensity exercise did not affect paired-pluse facilitation(PPF), but enhanced the hippocampal L-LTP in the CA1 region(P<0.05),(3) The expression level of hippocampal P-CREB showed a significant up-regulation(P<0.05) in the rats of EG. Conclusions: The results indicates that low intensity exercise can enhance the learning and memory ability of rats, and the underlying mechanisms may be associated with the enhancement of synaptic plasticity and the up-regulation of P-CREB in the hippocampus of rats.

关键词： Low intensity exercise learning and memory late phase long-term potentiation(L-LTP) cA MP response element-binding protein(CREB) synaptic plasticity

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Triptolide promotes α-synuclein degradation in neuronal cells by autophagic pathway

Triptolide promotes α-synuclein degradation in neuronal cel...

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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： Ting Zhang Guanzheng Hu Le Wang Yang Liu Xiaomin Wang Department of Neurobiology Capital Medical UniversityBeijing Institute for Brain Disorders and Key Laboratory for Neurodegenerative DisorderMinistry of Education

Parkinson's disease(PD) has become a social problem in China, seriously affecting population health and life quality and inhibiting economic development. However, no effective treatment for PD is available to control the disease progression. Our previous study shows that triptolide provides neuroprotective effect in different animal models of PD, but the mechanism is still unclear. In the present study, we transfected wild-type(WT) or A53 T mutant(A53T) α-synuclein in MN9 D cells for 24 h and added different concentrations of triptolide for another 24 h. We found triptolide reduced α-synuclein overexpression level in MN9 D cells. To test whether triptolide reduced the synthesis of α-synuclein, we observed the m RNA level of α-synuclein by RT-PCR assay and found triptolide has no effect, indicating triptolide promoted the degradation of α-synuclein. Considering the autophagy-lysosome pathway(ALP) and the ubiquitin-proteasome system(UPS) are both involved in the α-synuclein recycling, we added 3-MA, an inhibitor of autophagy, and lactacysin, an inhibitor of proteasome with triptolide and found 3-MA, but not lactacysin, abolished the inhibition effect of triptolide. Moreover, the level of p62 declined with α-synuclein expression, indicating autophagy machinery is involved in this process. These results provide the first evidence that triptolide may promote the clearance of α-synuclein inneuronal cells, which may help translate the application of triptolide from bench to bedside, as well as to advance our understanding of alternative medicine in the treatment of PD.

关键词： triptolide,autophagy,α-synuclein

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