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Synergic effects of constant high-speed rotation and rotating background on visual cognitive processing

Synergic effects of constant high-speed rotation and rotatin...

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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： Siyang He Peng Zou Linjie Wang State Key Laboratory of Space Medicine Fundamentals and Application China Astronaut Research and Training Center

The variations of visual cognitive processing under the complex condition of constant high-speed rotation and visual rotation backgrounds with different speed were explored in this study. 14 university students participated in the experiment. Rotary chair was used to create constant high-speed rotation. Two kinds of background were employed, and they were normal black background and simulated star background. Subjects were asked to perform selective switch response task when rotary chair and visual background were rotating simultaneously. Electroencephalogram(EEG) was recorded from 12 scalp sites. It was found that when rotary chair was rotating at 130°/s compared with the N1 latencies under 30°/s and 60°/s rotating backgrounds, the posterior N1 latencies were longer under black background. The P1 latencies under 30°/s rotating background were longer than that under black background. The P1 and N1 latencies were shortest under 45°/s rotating background and longest under 60°/s rotating background. The tendency that averageamplitudes of posterior N1 increased with the speed of rotating background disappeared, and was replaced by the highest average amplitudes of posterior P1 and N1 in 45°/s rotating backgrounds. Under 60°/s rotating background, average amplitudes of posterior P1 and N1 were the shortest. It was demonstrated that under high constant rotation the cognitive facilitate effect under normal environment was inhabited to some extent, and the disassociation between anterior and posterior N1 mean amplitudes was arisen with the influences of different background speed in selective switch response task. It was suggested that the anti-interference ability in prefrontal lobe decreased, but the recruitment of activated neurons in primary visual cortex was enhanced with the increased speed of rotating background. And it was also hinted increased arousal level and resources utilization efficiency under the complex cognitive context.

关键词： Brain event-related potentials N1 P1 rotating background constant high-speed rotation

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The protective effect of NMDA receptor inhibitors on nigral iron accumulation in 6-OHDA-induced Parkinson's disease models

The protective effect of NMDA receptor inhibitors on nigral ...

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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： Xiaodong Liu Jianjian Xia Huamin Xu Hong Jiang Junxia Xie Department of Physiology Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: PhysiologyMedical College of Qingdao University

Parkinson's disease(PD) is a neurodegenerative disease, which is mainly occurred in elderly person. The main pathological changes of PD are degeneration of dopamine(DA) neurons in the substantia nigra pars compacta(SNpc), thus resulting in the reduced release of DA in the striatum(Str). However, the precise pathogenic mechanisms leading to neurodegeneration in PD are not known. Increasing evidence has proved that elevated nigral iron levels played an important role in the etiology of PD. Our previous studies have shown that misregulation of iron transporters such as divalent metal transporter(DMT1) were involved in this nigral iron accumulation in PD. N-methyl-D-aspartate(N-methyl-D-asparate, NMDA) receptor is a glutamate receptor. It was reported that NMDA receptor-mediated excitatory toxicity was one of the important mechanisms contributed to the neurodegeneration of DA neurons in PD. Evidence also proved that iron chelator could inhibit NMDA receptor-mediated cytotoxicity in the primary cultured cortical neurons,and activation of NMDA receptor in rat hippocampal neurons could up-regulate the expression of DMT1, thus increase iron influx in the hippocampus. This indicated that there might be a correlation between the activation of NMDA receptor and iron metabolism. However, whether activation of NMDA receptors is involved in nigral iron accumulation in PD and the possible mechanisms are not known. Therefore, in the present study, 6-hydroxydopamine(6-OHDA) was used to induce PD rat models to elucidate the protective effect of NMDA receptor inhibitors including MK-801 and AP5 on nigral iron accumulation in6-OHDA-induced PD models. Using high-performance liquid chromatograph electrochemical detection(HPLC-ECD), immunohistochemistry, western blots and iron staining, we investigated the protective effects of MK-801 and AP5 on the SN-Str projection system and iron accumulation against 6-OHDA treatment. The results showed that NMDA receptor inhibitors MK-801 or AP5 could

关键词： NMDA receptor Parkinson's disease DMT1 MK-801 AP5

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Intranasal administration of Exendin-4 antagonizes circadian rhythm disorders induced by Aβ31-35

Intranasal administration of Exendin-4 antagonizes circadian...

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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： Qian-Qian Yu Li Wang Xue-Ling Zhao Yang Li Xiao-Hui Wang Department of Pathology Shanxi Medical University

Alzheimer's disease(AD)is a degenerative disorder of the central nervous system, which often impairs learning and memory, emotion and cognitive function. In addition, circadian rhythm disorders are obvious in early stage of AD and deteriorated gradually. Clock genes located in Suprachiasmatic Nucleus(SCN) regulate mammalian circadian rhythm. There are two most important genes, namely Per1 and Per2, which play crucial roles in circadian rhythm in mice. SCN can adjust sleep, affect behavior and metabolism and prompt organs to fit external environment via integrating neurological or endocrine signals into external rhythms. It was reported that Type 2 diabetes mellitus(T2DM) was similar to AD in pathogenesis and pathology. Exendin-4, GLP-1 analogue, had been already approved for the treatment of T2 DM currently. The study discussed that whether intranasal administration of Exendin-4 could modify circadian rhythm disorders of AD model mice and explored expression of clock genes at the molecular level in order to find a new, moreeffective method for the treatment of rhythm disorder. We injected Aβ31-35 into hippocampal CA1 region of mice by stereotaxic apparatus, observed wheel-running activity in control and AD mice separately under laboratory conditions of constant darkness(DD) by the test of wheel running. The study suggested that free-running period and sleep phase-motofacient phase were both disrupted in AD model mice. However, intranasal administration of Exendin-4 could reverse them partially. Further more, we removed SCN tissue at different circadian times(CT) and analyzed clock genes by qR T-PCR. The result showed that, compared with control group, the peak expression of Per1 and Per2 had been alterated in AD model mice. However, the expression of Per1 and Per2 after pretreatment with intranasal administration of Exendin-4 had been restored partially. The study provides behavioral and molecular biological evidence for circadian rhythm disorder in AD and lays nece

关键词： Alzheimer's disease circadian rhythm Exendin-4

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GDF-15 enhanced intracellular Ca2+ through the Akt/m TOR and ERK pathway-induced increase of Cav1.3 expression

GDF-15 enhanced intracellular Ca2+ through the Akt/m TOR 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： Chang-Ying Wang Jun-Mei Lu Yan-Jia Fang Yan-Ai Mei Institutes of Brain Science State Key Laboratory of Medical Neurobiology and School of Life SciencesFudan University

GDF-15 is a novel member of the transforming growth factor-β(TGF-β) superfamily, which plays critical roles in the central and peripheral nervous systems. We have previously reported that GDF-15 increased delay rectifier outward K+ currents(IK) and a-subunit Kv2.1 expression is likely through TβRII to activate the Src kinase and Akt/mT OR pathway in rat cerebellar granule neurons(CGNs). Here, we report that incubation of CGNs by GDF-15 for 24 h significantly enhanced the intracellular Ca2+ level evoked by high K+ stimulation measured by the calcium imaging. Similarly, GDF-15 also significantly increased inward Ca2+ current without modifying the properties of channels activity. The inhibition of L-type Ca2+ channels with nifedipine could reduce GDF-15-induced increase of intracellular Ca2+ level and inward Ca2+ current. Western blot analysis indicated that GDF-15-induced amplification of Ca2+ current was mediated by increasing the expression of the CaV1.3 a-subunit, but not CaV1.2. Similarly with our previous report, increase of CaV1.3 expression induced by GDF-15 is attenuated by inhibitors of Akt /mT OR and ERK pathway. Pharmacological inhibition of Src-mediated phosphorylation of TβRII rather than TβRI abrogates the effect of GDF-15 on CaV1.3 expression. Our data reveal, besides of increase of Kv2.1 expression, GDF-15 could increased CaV1.3 expression through TβRII to activate Akt/mT OR and ERK pathway, which is an unanticipated role of the non-Smad-dependent pathway similar with our previously characterized signaling mediated by GDF-15. Since voltage-gated L-type Ca2+ channels are key determinants of synaptic integration and plasticity and activity-dependent gene expression in neurons, our data will improves the important information for understanding the effect of GDF-15 on central neuron system.

关键词： GDF-15 Akt /mTOR and ERK pathway Ca2+ channels CaV1.3 CGNs

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Up-regulated expression of NT-3 mediated by hypoxia response element attenuates cerebral ischemia/reperfusion injury in rats

Up-regulated expression of NT-3 mediated by hypoxia response...

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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-Feng Zhang Li-Li Shi Li Zhang Peng-Bo Yang Jian-Shui Zhang Cun-Fang Qi Yong Liu Xi Xu Department of Anatomy Xi’an Medical University Institute of Neurobiology Xi’an Jiaotong University Health Science Center

To investigate the neuroprotective effects of neurotrophin-3(NT-3) expression controlled by five copies of the hypoxia-responsive elements(5HRE) after focal cerebral ischemia. Three groups of rats received RV-5H-NT3, RV-5H-EGFP or saline injection. Three days after gene transfer, the rats underwent 90 min of transient middle cerebral artery occlusion(t MCAO), followed by 1–28 days of reperfusion. Immunohistostaining and western blotting were performed to detect ischemia/hypoxia-regulated expression of NT-3 controlled by 5HRE. The volume of brain infarction and the apoptosis were analysised by TTC and TUNEL staining. The neurological scoring was determined by neurological behavior tests. Three days after t MCAO, brain NT-3 expression was significantly increased in the RV-5HNT3-transduced animals compared with the RV-5H-EGFP or saline group(P<0.05), and brain infarct volume was smaller in the RV-5H-NT3-transduced group than the RV-5H-EGFP or saline group(P<0.05). The percentage of TUNEL-positive cells was reduced in RV-5H-NT3-transduced brains compared with the RV-5HEGFP or saline group 3 and 7 days after t MCAO(P<0.05). Furthermore, the neurological status of RV-5H-NT3-transduced rats was better than that of RV-5H-EGFP- or saline-transduced animals from 1 day to 4 weeks after t MCAO(P<0.05). Our results demonstrated that 5HRE could modulate NT-3 expression in the ischemic brain environment and that the up-regulated NT-3 could effectively improve neurological status following t MCAO due to decreased initial damage.

关键词： hypoxia-inducible gene expression neuroprotection ischemic stroke gene therapy

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HMGN2 regulate the maintenance of neural stem cells in mouse embryonic neocortex

HMGN2 regulate the maintenance of neural stem cells in mouse...

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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： Xue-ling Gao Wen-jia Tian Peng-cheng Chu Qin Shen Tsinghua-Peking Center for Life Sciences Tsinghua University Center for Stem Cell Biology and Regenerative Medicine School of MedicineTsinghua University School of Life Sciences Peking University

Neural stem cells(NSCs) are capable of self-renewal and generate the major cell types in the brain. contributing to the complexity of the brain. Studies on the molecular mechanism controlling the development of neural stem cells will help us better understand the process of neural development and the causes of neurodevelopmental diseases. Although emerging evidence has shown that alternation of chromatin structure is an important way to regulate gene expression, few have been reported in the process of neural development. HMGN2(High Mobility Group Nucleosomal binding protein 2) is a highly conserved chromosomal binding protein across vertebrates. Despite the fact that HMGN2 is highly expressed in the embryonic mouse brain and that HMGN2 knock-out mice are reported embryonically lethal, the function of HMGN2 in embryonic development, especially in neurogenesis is barely studied. We found that HMGN2 was highly expressed in the germinal zone of the cerebral cortex throughout development starting from embryonic day 10(E10). but also in differentiating neurons in the cortical plate. Revealed by double labeling with cell-type specific markers. HMGN2 is abundant in neural stem cells and neuroblasts but almost absent in intermediate progenitor cells. Knocking down HMGN2 reduces the number of proliferative cells and stem cells in differentiating Ell neural stem cell culture. On the contrary overexpression of HMGN2 in vitro sustains neurospheres' formation and passage. We also analyzed the function of HMGN2 in vivo using in utero electroporation and knock-out mouse lines. To understand the molecular mechanism underlying the function of HMGN2 in NSCs, we investigated the change of chromatin conformation and histone modifications after HMGN2 knock-down by biochemical and molecular assays. Our study suggests that HMGN2 is an important modulator regulating NSC maintenance likely through an through an epigenetic control.

关键词： HMGN epigenetic embryonic neocortex neural stem cell

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Preliminary exploration the effect and mechanism of 1.84GHZ radio-frequency electromagnetic radiations (RF-EMR) on the cognitive behavior in C57 mice

Preliminary exploration the effect and mechanism of 1.84GHZ ...

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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： Kai Wang Lin-Qi Hu Yan-Ai Mei Institutes of Brain Science School of Life Sciences and State Key Laboratory of Medical NeurobiologyFudan University East China Normal University

With the growing popularity and widely used of mobile phones in recent years, it is increasingly concerned about whether the mobile phone radio frequency electromagnetic radiation(RF-EMR) affect human health. Mounting studies have noted that exposure to RF-EMR may both positively and negatively influence the learning and memory of rodents due to the different frequency and intensity of radiation used. In this study, we used a mouse model to examine the effects of shortly exposure to 1.84 GHZ RF-EMR for 30 min on a recognition memory task and electrophysiological recording in pyramidal neurons of mice prefrontal cortex. The data indicated that RF-EMR exposure induced a significantly and power-dependent increase in novel object associative recognition memory. This increase of cognitive index was observed without corresponding changes in spontaneous locomotor activity observed with the classic open-field test Moreover, 1.84 GHZ RF-EMR-induced increase of recognition memory can continue for 8 days at least while mice exposure to 150 W power for 30 min(distance 1.5 m). The data obtained from whole-cell patch clamp recording showed that exposure 1.84 GHZ RF-EMR(150 w for 30min) significantly reduced the half-width of cortical neuron action potential and the threshold which elicited action potential. The morphological changes in cortical neuron after exposure 1.84 GHZ RF-EMR is going on study. Our results demonstrated, for the first time, that exposure to 150 W of 1.84 GHZ RF-EMR for 30 min can significantly increase the recognition memory and cortical neuron excitability. However, since the 150 W RF-EMR level, which induced the increase of recognition memory and potential changes in neuron excitability in this study, is not within the general range in daily human lives, our study is thus more significant for elucidation of biological mechanisms than for human health risk assessment. Our data suggest that shortly exposure 1.84 GHZ RF-EMR may be as a potential therapeutic a

关键词： RF-EMR C57 mice cognitive index action potential

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In vivo firing patterns of medial septal cholinergic neurons and modulation of hippocampal activities

In vivo firing patterns of medial septal cholinergic 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： Xiao-yu Ma Li-na Wang Ce-qun Wang Yi-yao Zhang Long-nian Lin Key Laboratory of Brain Functional Genomics (Ministry of Education) Institute of Brain Functional GenomicsSchool of Life ScienceEast China Normal University

The medial septum is an important component of the basal forebrain cholinergic system. It provides the major source of cholinergic innervation to the hippocampus and plays a part in hippocampal-dependent functions such as learning and memory. Despite the vital role of medial septal cholinergic neurons, limited information is known about their in vivo firing patterns as well as physiological functions. Combining multichannel in vivo recording techniques and optogenetics, we aimed to study the firing properties of medial septal cholinergic neurons and their modulatory effects on hippocampal activities in choline acetyltransferase-channelrhodopsin2(Ch AT-Ch R2) mice. In the medial septum of Ch AT-Ch R2 mice, immunohistochemistry showed that 98.5 ± 3.4% of the Ch R2-expressing neurons co-expressed Ch AT, and 75.4 ± 14.9% of the ChA T-expressing neurons co-expressed Ch R2. Whole-cell patch-clamp recordings in brain slices reveled that neurons expressing Ch R2 could be activated by 473 nm blue light. To study the in vivo firing patterns of medial septal cholinergic neurons, we designed optic fiber-bonded microdrive arrays so that light pulses could be delivered to recording sites. We recorded 10 neurons that responded to blue light stimulation in the medial septum from 7 freely behaving mice. We determined these were Ch AT-expressing neurons, that is, cholinergic neurons. Based on their in vivo firing patterns, these 10 neurons were divided into two groups. Firing activities of typeⅠcholinergic neurons were closely related to hippocampal theta rhythm. Across theta states such as active exploration and rapid eye movement sleep, this type of neurons were much more active, with mean firing rates at 7.7 ± 1.2 Hz during active exploration and 3.1 ± 1.0 Hz during rapid eye movement sleep. Across non-theta states such as slow-wave sleep, this type of neurons were less active, with the mean firing rates dropping to 0.4 ± 0.6 Hz. On the other hand, mean firing rates of typeⅡcholin

关键词： medial septum cholinergic neurons theta sharp wave-ripple in vivo

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Embryonic NMDAR blockade induces anxiety-like behavior by interrupting NMDAR development in both hippocampus and prefrontal cortex

Embryonic NMDAR blockade induces anxiety-like behavior by in...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Wan-ting Ren Long-zhen Cheng Xiao-ling Liu Li-chao Peng Yun Wang Institutes of Brain Science & State Key Laboratory of Medical Neurobiology Department of AnaesthesiaThe Fifth People’s Hospital of ShanghaiFudan University The Department of Anaesthesia The People’s Hospital of Huangshan

Postnatal NMDA receptor(NMDAR) blockade causes neuronal deficient in adolescence and adult life. However, the influences of interruption of NMDAR function during early embryonic period on the NMDAR development in hippocampus and its projective region—prefrontal cortex still remain unknown. In this study, we treated the E14 pregnant rats with NMDAR blocker ketamine for 5 consecutive days to explore the modification of NMDAR function and the behavior performance in their offspring. Using the electrophysiology, western blotting and behavioral test, we discovered that ketamine treatment significantly enhanced the NMDAR functional development curve in hippocampal CA1 neurons during first 4 weeks of postnatal life. This is likely due to the over expression of the cell membrane NR2 B containing NMDARs and the enhanced proportion of p-NR2BTyr1472. The patchclamp study also revealed that the enhanced NMDA current in ketamine treated offspring was significantly inhibited by the selective NMDAR-2B antagonists. However, the degree of NMDAR functional enhancement in hippocampus was reduced when the offspring rats reached to adult life(postnatal week 8). Interestingly, at the same time period, NMDA current was significantly reduced in prefrontal cortex, in which no difference had found in juvenile. By employing the NMDAR-2A or NMDAR-2B antagonist separately in NMDA current detection, we found this reduction of current may induce by the attenuated function of NR2 A, consistent with the evidence of NR2 A membrane expression decrease. Moreover, ketamine treated offsprings showed anxiety-like behavior in elevated-plus maze test in adulthood, but not in juvenile. In conclusion, embryonic NMDAR blockade with ketamine altered the NMDAR development process with a selective enhancement of NR2 B expression and function in juvenile hippocampus, and subsequently attenuation of NR2 A mediated NMDAR function in adult prefrontal cortex, which may induce anxiety-like behavior.

关键词： NMDAR hippocampus prefrontal cortex anxiety

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Triptolide induces autophagy and protects dopaminergic neurons against MPP+ damage

Triptolide induces autophagy and protects dopaminergic neuro...

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

Triptolide is a monomeric compound isolated from a traditional Chinese herb, tripterygium wilfordii Hook.f.(TWHF). It has been identified as the major components in TWHF to exert immuno-suppressive, anti-inflammatory, antifertility, and antitumor activities, as well as neurotrophic and neuroprotective effects. In our previous research, it has been demonstrated that triptolide revealed a significant protective effect in various Parkinson's disease(PD) models. More and more studies indicates that autophagy is involved in PD process and rapamycin, an agonist of autophagy, can protect against DA neuron damage in PD models. It is also reported that triptolide can increase the expression of LC3-II protein and the number of autophagosome in pancreatic cancer cells. So we want to know the relationship between triptolide and autophagy in protecting dopaminergic neurons. To identify the direct relationship between triptolide and autophagy, we treated MN9 D cells or primary rat neurons with different concentrations of triptolide for 24 h, and observed the expression level of LC3-II, an autophagy specific marker, by Western blotting. We found that triptolide increased LC3-II level in both MN9 D cells and primary rat neurons, without affecting LC3-I levels. In addition, we examined the ultrastructural changes in MN9 D cells using Transmission electron microscopy(TEM), and found increased numbers of autophagosome after triptolide treatment. Moreover, by using chloroquine(CQ), a lysosome inhibitor, we found triptolide didn't influence the autophagic flux in MN9 D cells. Most importantly, in MPP+ induced MN9 D cells, pretreatment of triptolide could increase the cell viability compared with control group. These results indicate triptolide induces autophagy in neurnal cells and protects the cells against MPP+ damage.

关键词： triptolide autophagy Parkinson's disease

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