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Rab5 dependent membrane endocytosis is required for Semaphorin3A induced axon growth cone collapse

Rab5 dependent membrane endocytosis is required for Semaphor...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Kong-Yan WU~1,Ai-Li SHENG~1,Wen-Wen LIU~2,An-Qi GENG~1,Xing-Yu JIANG~2,Xiao-Bing YUAN~1, Zhen-Ge LUO~(1,*) 1 Institute of Neuroscience,State Key Laboratory of Neuroscience,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences,Shanghai 200031,China 2 CAS Key Lab for Biological Effects of Nanomaterials and Nanosafety,National Center for NanoScience and Technology,Beijing 100190,China

Guidance cues are critical for axon navigation and ultimately for the wiring of the neuro-circuits during nervous system *** cones of growing axons can sense both attractive and repulsive cues in the environment and make a corresponding ***3A,a negative guidance cues,can collapse growth cones of outgrowing axons,however,the intracellular molecular mechanisms are not well *** we show that the small GTPase Rab5 is involved in growth one collapse in response to ***5 activity assay shows that Rab5 is transiently activated after treatment with *** cone collapse is abolished by down-regulation of Rab5 by specific siRNA in response to *** advantage of live cell FRET assay,we demonstrate that semaphorin3A can activate Rab5 and promote the retrograde trafficking of Rab5 positive endosomes in growth ***5 is required for endocytosis of the growth cone plasma membrane during growth cone collapse. Over-expression of Rab5 leads to axon growth cones collapse in vitro and impedes projecting axons growth in vivo. These findings indicate that in response to negative guidance molecules semaphorin3A,axon growth cones driving endocytosis of the plasma membrane associated with the activated function of Rab5 resulted in growth cone collapse.

关键词： growth cone Semaphorin3A Rab5 endocytosis plasma membrane FRET microfluidic culture system electroporation

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The protection of EphrinB in the rat hippocampus after transient forebrain ischemia and reperfusion

The protection of EphrinB in the rat hippocampus after trans...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Ye WANG,Nai-Hong LIU,Rui WANG,Jian-Guo LI~*,Ce ZHANG~* Department of Physiology National Key Disciplines,Key Laboratory for Cellular Physiology of Ministry of Education,Shanxi Medical University,Taiyuan 030001,China

Objective Transient forebrain ischemia-reperfusion induces delayed,selective neuronal death in the CA1 region of the *** studies have consistently demonstrated that overactivation of the NMDA subtype of glutamate receptors is the primary step leading to neuronal injury after insults of stroke and brain ***, the underlying mechanisms of the overactivation of NMDA receptors in this case remain *** Eph family of receptor tyrosine kinases(comprising EphA and EphB receptors),along with their ephrinA or ephrinB ligands,play an essential role in regulating the properties of synapses including modulating NMDA *** present study thus explored the effects of ephrins on ischemia-reperfusion-induced delayed neuronal death in the CA1 region by modulating NMDAR *** Transient forebrain ischemia(15 min) was induced by the use of the four- vessel occlusion method with some *** 24 h and 48 h after reperfusion,hippocampal regions of adult rats were treated for western blot or TUNEL *** In the present study,we found increased expression of ephrinB2,p-NMDA receptors and pERKl/2 in CAl neurons at 24 h and 48 h after ischemia and *** of ERK1/2 with U0126 attenuated the increased expression of ephrinB2,p-NMDA receptor and delayed neuronal cell *** This study provides an evidence for the ephrinB in protection of neuronal damage in vulnerable CAl ***-ephrin system thus would be a therapeutic target against the ischemia-induced neuronal damage.

关键词： ephrinB2 ischemia delayed neuronal death hippocampal neuron rats

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Localization of molecular determinants in sensitivity of sodium channels to BmK I probing by surface plasmon resonance assay

Localization of molecular determinants in sensitivity of sod...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Pin YE,Xing-Hua FENG,Hong-Tian YANG,Yong-Hua JI~* Lab of Neuropharmacology and Neurotoxicology,Shanghai University,Shanghai 200444,China

Previously,domain IV S3/S4 linker was demonstrated to be an important region determing the sensitivity of sodium channels to BmK I,a sodium channel-specific site-3 *** the localization of molecular determinants in sensitivity of sodium channels to BmK I remained *** this study,through channel alignment,DIV/S3-S4 linker in BmK I-insensitive rNav1.8 was inserted by two amino acids(LE) compared with *** constructing channel mutants mimicing the rNav1.8 DIV S3/S4 region in rNav1.5 backbone,the sensitivity of rNav.15 mutants to BmK I was remarkably ***,two peptides were synthesized according to the DIV/S3-S4 linker in rNav1.5(peptide P1) and rNav1.8(peptide P2).The binding affinities of peptides to BmK I was investigated by surface Plasmon resonance(SPR).The results showed that both P1 and P2 could bind with BmK *** there were significantly differences in binding capability between these two *** binding response(RU) of the peptide P2 was reduced to about 1/3 of the peptide *** association kinetics of P2 was also *** was presumed that the insensitivity of sodium channels to BmK I could be attributed to the alteration of microstructure of the receptor site by LE ***,it may provide cludes for the diversity of spatial structure of receptor sites mapping for BmK I-sodium channel interaction.

关键词： sodium channels surface plasmon resonance BmK I

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Amygdala neurons encode fear and anxiety

Amygdala neurons encode fear and anxiety

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Long-Nian LIN Key Laboratory of Brain Functional Genomics(Ministry of Education and Shanghai),Institute of Brain Functional Genomics,East China Normal University,Shanghai 200062,China

Fear and anxiety both produce similar responses to certain *** is an emotional response to an imprecise or unknown threat,and fear is an affective response to a real threat or *** amygdala has been proposed to play an essential role in the mediation of emotions such as fear and ***,the neural coding mechanisms underlying fear and anxiety in the amygdala are not *** using multi-channel recording techniques,we investigated the neuronal activity in the mouse amygdala responding to various threatening contexts. Here we report that in freely behaving mice,one group of neurons in the basolateral amygdala(BLA) could respond to diverse menaces such as heights and moving *** baseline firing rates of these neurons were remarkably low,about(0.1±0.12) Hz.A subset of these neurons can be selectively activated by fear of *** firing rates increased dramatically[(11.39±0.86) Hz]when mice stayed on an elevated platform(10 cm long,7 cm wide,and 10 cm high);their firing rates could reach 50 Hz when mice fell from a high *** subset of these neurons was sensitive to the movement regardless of other properties of *** neurons could respond to all kinds of moving objects,such as moving toys,shaking hands,and flashing characters on the computer *** firing rates increased significantly to 30-60 Hz when given strikingly different moving *** group of neurons in the BLA fires tonically under anxiety conditions in both open-field and elevated plus-maze *** firing patterns of these neurons displayed a characteristic slow onset and progressively increased firing ***,these firing patterns were correlated to a gradual development of anxiety-like behaviors in the open-field ***, these neurons could be activated by any impoverished environment similar to an open-field;and introduction of both comfortable and uncomfortable stimuli temporarily suppressed the activity of t

关键词： amygdala fear anxiety neural coding

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Vangl2 regulation in a mammalian model for planar polarity

Vangl2 regulation in a mammalian model for planar polarity

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Arnaud Giese La Lasvaux Claire Mazzocco Elodie Richard Matthew W.Kelley Nathalie Sans John Brigande Mireille Montcouquiol INSERM U862 Neurocentre MagendiePlanar Polarity and Plasticity groupBordeauxFrance University of Bordeaux France

Vangl2 is one of the central proteins controlling the establishment of Planar Cell Polarity in different tissues and ***,results in both flies and mammals suggest that that the localization of Vangl2 protein to specific intracellular microdomains is crucial for normal ***,the molecular mechanisms that control Vangl2 trafficking within a cell are largely ***,we identify a new binding partner for Vangl2,G-protein signaling-GAIP -interacting protein 1(GIPC1).We show that the central PDZ domain of GIPC1 directly associates with the last 12 amino acids of Vangl2,and that GIPC1,along with the motor protein MyosinⅥ(MyoⅥ),co-localizes with Vangl2 in endosomal *** show that a GIPC1/MyoⅥcomplex regulates the levels of Vangl2 at the plasma membrane. Consistent with this result,high resolution imaging by STED microscopy reveals a depletion of Vangl2 in the proximal membrane of hair cells,a location with a large accumulation of ***,downregulation of GIPC1 in hair cells by shRNA in vitro or in utero leads to hair cell maturation defects,including defects in hair bundle orientation and *** results demonstrate a role for GIPC1 in the regulation of Vangl2 protein within developing hair cells. Moreover,morphological analysis of the effects of depletion of GIPC1 indicates a broader role for this molecule in the development of both stereociliary bundles and planar cell polarization.

关键词： planar polarity inner ear traffic cochlea Van Gogh-like 2

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Fast nongenomic neuroprotection mediated by GPR30-dependent depression of NR2B-containing NMDA receptors

Fast nongenomic neuroprotection mediated by GPR30-dependent ...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Nan ZHANG,Ming-Gao ZHAO~* Department of Pharmacology,School of Pharmacy,Fourth Military Medical University,Xi'an 710032,China

17-β-Estradiol(E2) is a steroid hormone involved in neuroprotection against excitotoxicity and other forms of brain *** genomic and non- genomic mechanisms,E2 modulates neuronal excitability and rapidly increases signal transmission by regulating N-methyl-D-aspartate(NMDA) and non-NMDA *** potential neuroprotective role of estradiol in chronic neurodegenerative disorders and acute brain ischemia following cardiac arrest and stroke is of great therapeutic ***,the mechanisms and identity of the receptors involved remain unclear,although it has been suggested that G-protein-coupled receptor 30(GPR30) is linked to protection against ischemic *** this study,rapid nongenomic neuroprotection by GPR30 stimulation was examined in culture cortical *** E2 and the GPR30 agonist Gl attenuated the excitotoxicity induced by NMDA receptor *** acute neuroprotection induced by GPR30 stimulation was dependent on G-protein coupled signaling and ERK1/2 activation,but independent of gene transcription and protein *** of GPR30 by transfection with small interfering RNAs(siRNAs) significantly reduced E2-induced rapid neuro- *** recordings revealed that the activation of GPR30 significantly depressed exogenous NMDA-elicited currents. Short-term activation of GPR30 did not affect expression of either NR2A- or NR2B- containing NMDARs;however, it depressed the phosphorylation of the NR2B subunit at *** findings provide direct evidence that fast nongenomic neuroprotection by estradiol is mediated by GPR30 stimulation and ensuing down-regulation of NR2Bcontaining *** of NMDAR activity by GPR30 stimulation may be an important mediator of estradiol-dependent neuroprotection.

关键词： N-methyl-D-aspartate receptor G-protein-coupled receptor 30 neuroprotection

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Neural correlates of spatial frequency-dependent stimulus contrast detection in cat

Neural correlates of spatial frequency-dependent stimulus co...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Tian-Miao HUA~(1,*),Xia-Ming SHI~1,Guo-Peng HUA~1,Zhong-Lin LU~(2,*) 1 School of Life Sciences,Anhui Normal University,Wuhu 241000,China 2 Laboratory of Brain Processes(LOBES),Departments of Psychology and Biomedical Engineering and Neuroscience Graduate Program,University of Southern California,Los Angeles,CA 90089,USA

Objective Contrast sensitivity to visual stimulus shows an evident dependency on stimulus spatial frequency in many species of *** neural basis remains ***,we investigated the role of primary visual cortex(V1:area 17) in spatial frequency-dependent contrast *** The perceptual contrast sensitivity functions(CSF) of three cats were measured using a two-alternative forced choice(2AFC) *** responses of V1 neurons to their optimal visual stimuli in a range of luminance contrast levels(from 0 to 1) were recorded subsequently using in vivo extracellular single-unit recording *** contrast sensitivity of each neuron was *** neuronal CSF in each cat was constructed from the mean contrast sensitivity of neurons at different preferred spatial ***(1) The perceptual and neuronal CSFs in all three cats exhibited a similar shape with a peak near 0.4 c/deg.(2) The neuronal CSF of each cat was highly correlated with its perceptual CSF.(3) V1 neurons responding preferentially to stimuli at different spatial frequencies had different contrast-gain. Conclusion(1) Visual contrast detection at different spatial frequencies may likely involve population coding of V1 neurons with different preferred spatial frequencies.(2) Differences in contrast-gain may underlie the observed contrast sensitivity variation of V1 neurons with different preferred spatial frequencies,resulting from long-term biological evolution or postnatal visual experience.

关键词： contrast detection neural correlates visual cortical neurons cat

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Early-stage epileptogenesis and intervention

Early-stage epileptogenesis and intervention

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Sheng-Tian LI School of Life Sciences and Biotechnology,Shanghai Jiao Tong University,Shanghai 200240,China

Objective Over 30%of people with epilepsy are not responsive to the treatment even to the best available ***,it is of great theoretical and clinical significance to investigate the mechanisms underlying epilepsy,and to search for effective *** reports have shown that N-methyl-D-aspartate（NMDA） receptors are extensively involved in epilepsy genesis and ***,few studies have focused on the role of extrasynaptic NMDA receptors in ***,in the present study we analyzed extrasynaptic NMDA receptor-mediated currents during the early stage of *** is a fundamental molecule in cells, which has been shown to decrease oxidative and excitotoxic cell death as well as ischemic brain *** the current study,therefore,we also tested the effect of NAD on pilocarpine-induced *** Adult C57BL/6 mice models of pilocarpine-induced epilepsy were established,and hippocampal slices were prepared at 24 h after the onset of status epilepticus（SE）.Changes in synaptic and extrasynaptic NMDA receptor-mediated excitatory postsynaptic currents（NMDA-EPSCs） were recorded in CA1 pyramidal neurons by whole-cell patch clamp technique. On the other hand,NAD or vehicle was *** 1 h after the onset of pilocarpine-induced *** of spontaneous recurrent seizures（SRS） was recorded by EEG recording technique in freely moving mice at two weeks ***（1） There were no significant differences in synaptic NMDA-EPSCs between pilocarpine and control groups in terms of rise time and decay time.（2） The peak amplitudes and rise time of extrasynaptic NMDA-EPSCs were not statistically different between the two groups.（3） Extrasynaptic NMDA-EPSCs decay was significantly faster in the pilocarpine-treated mice.（4） NAD treatment markedly decreases the number of spontaneous epileptiform EEG activity.（5） Histological experiments showed that NAD treatment reduces the brain injury in the pilocarpineinduced e

关键词： epilepsy NMDA receptor extrasynaptic NAD+

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Anisotropic neuro-mechanical compensation for kinematic variability in multi-joint arm postural control

Anisotropic neuro-mechanical compensation for kinematic vari...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Xin HE,Yu-Fan DU,Xin WANG,Ning LAN~* Laboratory of Neuro-modulation and Modeling,Institute of Rehabilitation Engineering,The Med-X Research Institute, School of Biomedical Engineering,Shanghai Jiao Tong University,Shanghai 200030,China

Objective The purpose of this study is to analyze the efficiency of neuro-mechanical compensation for kinematic variability during postural *** dependent noise(SDN) in natural neuromuscular recruitment brought intrinsic instability in posture maintaining ***,random drifting of human arm endpoint was substantially suppressed by neuro-mechanical compensation and reflex regulation in normal subjects,and it may become notable in pathological conditions like Parkinson's *** the efficiency of neuro-mechanical compensation for kinematic variability may help us find out the control principals our brain adopted in position control,and maybe helpful for rehabilitation treatment planning for patients with motor *** We use a realistic virtual arm(VA) model to address this issue through a computational *** properties at muscle, joint,and hand coordinates were evaluated to obtain an estimation of mechanical *** between muscle stiffness and SDN were simulated with simple patterns of feedfoward activation of *** resultant stiffness and drifting in hand were analyzed by principal components and characterized by elliptic *** (1) The extent of random hand drifting ellipse was inversely modulated by the hand stiffness ellipse.(2) Higher levels of muscle activation caused anisotropic increases of hand stiffness mainly in the major axis direction,consequently leading to anisotropic growth of hand drifting.(3) A U-shaped ratio against total muscular energy consumption between the area of hand endpoint stiffness ellipse and that of hand endpoint drifting ellipse,therefore,suggests thai it may not be efficient to counteract internal neural noise by using high levels of muscle stiffness(activation) in multijoint *** A suitable level of muscle stiffness may be optimal in maintaining a steady arm posture with minimal variation.

关键词： muscle stiffness neural noise kinematic variability multi-joint arm posture control

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The role of desensitization of G-protein-activated inward rectifier potassium(GIRK) channels in the development of febrile seizure

The role of desensitization of G-protein-activated inward re...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Ying-Ying WANG~1,Jiong QIN~(1,*),Ying HAN~1,Jie CAI~2,Guo-Gang XING~(2,*) 1 Department of Pediatrics,Peking University First Hospital,Beijing 100034,China 2 Neuroscience Research Institute and Department of Neurobiology,Peking University,Beijing 100191,China

Febrile seizures（FS）,or fever-induced seizures,are the most common form of seizures during childhood and have been associated with an increased risk of epilepsy later in *** has been suggested that hyperthermia （temperature of≥38.4℃） during fever plays a crucial role in generation of ***,the mechanisms underlying the pathogenesis of hyperthermia-induced seizures are poorly *** previous studies,we and others have suggested that GABA receptors are likely to be associated with *** this study,by using whole-cell patch-clamp recording techniques,we demonstrated that hyperthermia（39-40℃） provoked a "febrile seizure-like event" expressed as spontaneous,recurrent,epileptiform discharges（SREDs） followed by a series of sustained depolarizations（SDs） in cultured rat cortical neurons（7-14 DIV）.The SREDs were characterized by abruptly developing,paroxysmal depolarizing shifts（PDS） of membrane potential with high-frequency spike firing characteristic of electrographic *** also induced persistent neuronal hyperexcitability as assessed by their intrinsic electrogenic characteristics,including decreased:baseline resting potential（RP）,input resistance(R),amplitude,duration and afterhyperpolarization（AHP） of spontaneous action potentials and,decreased absolute value of the threshold potential （TP） and threshold current(I) for evoking the cell firing,shortened duration,decreased inter-spike intervals（ISI） as well as increased firing frequency of evoked action ***（100μM）,a specific GABA receptor agonist, significantly repressed the hyperthermia-induced neuronal hyperexcitability and epileptiform discharges in cultured cortical neurons,and these effects were prevented by treatment with the GABA receptor antagonist phaclofen. Moreover,hyperthermia elicited fast desensitization of G-protein activated inwardly rectifying K（GIRK） channels in cultured cortical neurons,whereas overexpression of GIRK1 and GIRK2 genes in cultured cortical

关键词： febrile seizures epileptiform discharges hyperthermia GABAB receptors GIRK channels cortical neurons

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