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Evoked-bursting from injured dorsal root ganglion neurons might act as a tactile allodynia pain signal

Evoked-bursting from injured dorsal root ganglion neurons mi...

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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 SONG~(1,2),Hui-Ming LI~1,Zhi-Feng YUE~1,Rou-Gang XIE~1,Xue-Jun SONG~3,San-Jue HU~(1,*),Jun-Ling XING~(1,*) 1 Institute of Neuroscience,Fourth Military Medical University,17 Chang-Le West Road,Xi'an,710033,China 2 Department of Physiology,School of Anesthesiology and Jiangsu Province Key Laboratory of Anesthesiology,Xuzhou Medical College,Xuzhou,221000,China 3 Department of Neurobiology,Parker University Research Institute,2500 Walnut Hill Lane,Dallas,Texas,75229,USA

Objective Tactile allodynia is one of the common features of peripheral neuropathy in which myelinated Aβfibers were proven to have contributed to the behavior in animal models and patients in previous *** firing patterns have been observed in Aβfibers,though the specific firing pattern which might mediate tactile allodynia remains poorly understood.A kind of evoked-bursting（EB） was identified on Aβneurons on a neuropathic pain model, the present study is to explore the characteristics of EB,whether there are causal link between EB and allodynia,and also the ion mechanism underlying the *** Chronic compression of dorsal root ganglion（DRG） models （CCD model） were prepared for tactile allodynia *** vivo intracellular recording,extracellular recording and in vitro patch-clamp recording were used for the observation of activity of DRG neurons and wide dynamic range （WDR） *** In CCD models,dominant tactile allodynia could be *** DRG soma became hyperexcitable with various firing patterns,in which,EB（a periphery input spike followed by the somatic burst firing） was identified on Aβneurons with a significantly increased percentage of 43.3%compared to normal neurons （13.3%）.Similar with spontaneous-bursting,a frequently observed firing pattern,the duration of EB increased with the membrane potential depolarization,and the existence of EB relied on the membrane potential oscillation.A distinct feature of EB is its dependence on periphery input especially from Aβafferent,which should be a prerequisite for the production of tactile ***-discharge of spinal cord WDR neurons in response to peripheral Aβstrength stimulation was a distinguishing feature of spinal neural correlate of tactile *** response was suppressed after abolishing EB at DRG level,thus,we propose that EB from injured DRG neurons might act as a tactile allodynia pain *** further investigated the ion current mechanism underlying *** c

关键词： dorsal root ganglion tactile allodynia wide dynamic range neuron evoked-bursting neuronal model

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Neuroprotective effects of BayK8644 against ischemic neuronal death in vivo and in vitro

Neuroprotective effects of BayK8644 against ischemic neurona...

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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： Feng-Qing HOU~#,Hong-Hai HU~#,Xin-Hong ZHU~*,Tian-Ming GAO~* Department of Neurobiology,Southern Medical University,Guangzhou 510515,China.

Stroke is the leading cause of disability and the third cause of death in the ***,underlying mechanisms of neuronal death induced by ischemic brain injury remain unclear and treatments for stroke are limited, mainly because of the short therapeutic window for *** Ca very early plays critical role in neuronal death induced by brain ischemia,activation of L-type Ca channel effectively triggers a group of genes required for neuronal survival and the currents mediated by L-type Ca channel indeed decreased in CAl neurons 24 h after forebrain *** we showed that L-type Ca channel agonist,BayK.8644 produced neuroprotective effects in oxygen-glucose deprivation（OGD） and forebrain ischemic animal *** present study,by using these two models,we tested the extended therapeutic window of BayK8644 for treatment of ischemic brain injury and the involved mechanisms were also *** found that in OGD model,BayK.8644（0.5 uM） administrated at 1 h,3 h,6 h,12 h after reoxygenation could reduced the neuronal death by 61.8%,52.9%,58.8%,61.6%,respectively;and L-type Ca channel blockers,nifedipine（10μM） and nimodipine（10 uM） could completely blocked the effect of *** nifedipine and nimodipine had no effect neuronal survival when they were given at 12 h after *** the transient forebrain ischemia model,injection of BayK8644（0.2 mM）(i.c.v.),even at 24 h after ischemia/ reperfiision,significantly increased the density of neurons that survived in the CAl region at hippocampus on the 7 day after ***,BayK8644 ameliorated severe deficiencies in spatial cognitive performance induced by transient global *** further characterize the underlying mechanisms of the neuroprotective effects of BayK8644,the activations of P38,JNK,ERK after OGD were first detected by using Western Blot and we found that the phosphorylations of P38 and JNK were enhanced at 30 min after OGD and restored to the normal level later. Most interes

关键词： L-type Ca2+ channel neuroprotection ischemia ERK

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Modulation of KCNQ potassium channels by a novel opener pyrazolo[l,5-a]pyrimidin-7(4H)-one compound QO-58

Modulation of KCNQ potassium channels by a novel opener pyra...

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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： Fan ZHANG,Jing-Jing MA,Yi MI,Jin-Long QI,Qing-Zhong JIA,Xiao-Na DU,Hai-Lin ZHANG 1 Department of Pharmacology,2 Department of New Drug Development,Hebei Medical University,Shijiazhuang 050017,China

Voltage-gated Kv7/KCNQ/M-potassium channels play an essential role in setting the resting membrane potential and in controlling the excitability of *** or depression of KCNQ channels results in neuronal hyperactivity and *** function is also indicated in nociceptive sensory ***,modulation of KCNQ2/3 function represents a potentially new strategy to treat neuronal excitability disorders such as epilepsy and neuropathic *** designed and synthesized a novel serial compounds of pyrazolo[1,5-a]pyrimidin-7（4H）- ones（PPOs）which activate KCNQ ***,in this study,we characterized one of these compounds,QO- 58's effect and mechanism underlying the activation of KCNQ channels using patch clamp technique.（1）QO-58 activated KCNQ2/Q3 currents at-40 mV concentration-dependently with a ECof 2.3±0.8μM.（2）QO-58 shifted the voltage-dependent activation of the KCNQ2/Q3 channel,and the Vwas shifted approximately-40 mV towards more negative potential in the presence 10 uM QO-58.（3）QO-58 significantly slowed channel activation and deactivation kinetics.（4）Among KCNQ channels,QO-58 increased homomeric KCNQ1-4 and heteromeric KCNQ3/Q5 currents recorded at-40 mV;The ECs value were 7.05±1.0,1.31±1.0,9.70±2.4,0.60±0.1,5.16±2.2μM,for KCNQ1, KCNQ2,KCNQ3,KCNQ4 and KCNQ3/Q5,respectively.（5）QO-58 enhanced native M currents from rat DRG neurons.（6）QO-58 dose-dependently prevented seizures induced by electroshock in rats,with a 73.3%reduction of seizures obtained at a dose of 50 mg/*** results indicate QO-58 is a potent KCNQ channel opener with more selective effect on KCNQ2 and ***-58 activates KCNQ channels through enhancing voltage-dependent activation and slowing channel ***-58 shows potent anti-seizure effects and can be developed further to treat disease related with neuronal hyperexcitability.

关键词： KCNQ channels M channel opener QO-58 seizures

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High glucose exacerbates β-amyloid production and the beneficial role of benfotiamine in vitro

High glucose exacerbates β-amyloid production and the benef...

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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： Xiao-Jing SUN,Lei ZHAO,Na ZHAO,Chun-Jiu ZHONG~* Department of Neurology,Zhongshan Hospital & Shanghai Medical College State Key Laboratory of Medical Neurobiology Institute of Brain Science Fudan University.

Our previous study has demonstrated that benfotiamine,a protective agent for diabetes complications, significantly decreases p-amyloid(Aβ) production through enhancing the phosphorylation levels and reduced enzymatic activities of both GSK-3αand GSK-3βin the APP/PS1 transgenic *** evidence from a population- based study also shows a link between Alzheimer's disease(AD) and diabetes mellitus(DM).The prevelance rate of AD is high as much as 2 to 5 times in population suffering from DM compared with non-DM control subjects. Experimental investigations suggest that the abnormality of cerebral glucose metabolism is the key etiological factor for *** we explored the effect of benfotiamine on high glucose exacerbating Aβproduction and the possible mechanism using HEK293 APPsw overexpression *** results showed that Aβproduction was first rising and then dropping along with the increased concentrations of glucose in the cell culture medium(1 g/L,3 g/L,4.5 g/ L,5.5 g/L,6.5 g/L,7.5 g/L,8.5 g/L,10.5 g/L) and the prolongation of incubated time(6,12,and 24 h).After being incubated for 6 h or 12 h,the Aβproduction of cells incubated in 5.5 g/L glucose was higher significantly compared with those of cells in 1 g/L glucose(6 h,P<0.05;12 h,P<0.01).It was associated with high glucose up-regulating the activities of GSK-3:The ratios of p-GSK-3a/GSK-3a and p-GSK-3β/GSK-3βin 5.5 g/L group were significantly decreased(p-GSK-3α/GSK-3α,P<0.01;p-GSK-3β/GSK-3β,P<0.05),and the activities of GSK-3a and GSK- 3βwere significantly increased compared with those in 1.0 g/L group(P<0.05).Benfotiamine significantly reduced Aβproduction enhanced by high glucose compared with control group(20 ug/mL group P<0.05,40μg/mL group P<0.01).The mechanisms may be through modulating GSK-3 activities:Benfotiamine(40μg/mL) significantly decreased the activities of GSK-3a and GSK-3βcompared with control group(P<0.05).Increased Aβproduction induced by high glucose is associated with the up-regulatio

关键词： Alzheimer's disease diabetes mellitus benfotiamene glycogen synthase kinase-3

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A role for orexin in central vestibular motor control

A role for orexin in central vestibular motor control

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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： Jun ZHANG~(**),Bin LI~(**),Lei YU,Ye-Cheng HE,Hong-Zhao LI,Jing-Ning ZHU~*,Jian-Jun WANG~* Department of Biological Science and Technology and State Key Laboratory of Pharmaceutical Biotechnology,School of Life Sciences,Mailbox 426,Nanjing University,22 Hankou Road,Nanjing 210093,China

The last decade has witnessed significant advances in our understanding of the physiological roles of orexin （also known as hypocretin）,a novel neuropeptide first identified in *** a neurotransmitter system originating uniquely from the lateral hypothalamus/perifornical area but projecting extensively to almost the whole brain,the central orexinergic system has been implicated in many basic nonsomatic functions,including the sleep/wake states, feeding,and reward ***,whether the central orexinergic system has a role in somatic motor control remains ***,orexin deficiency in humans,dogs,and rodents results in cataplexy,a motor deficit characterized by sudden loss of muscle tone,highlighting the possibility of a modulatory role for orexin in motor ***,since cataplexy is closely related to narcolepsy and often triggered by strong emotions,whether the effect of orexin on motor system is secondary to its actions on the neural circuits controlling sleep or emotions is not *** the present study,to reveal the exact relationship between the central orexinergic system and motor control, the effects of orexin on the lateral vestibular nucleus（LVN）,which holds a key position in control of muscle tone and posture and receives orexinergic innervation,and the underlying mechanisms were investigated at molecular, cellular,and behavioral ***,RT-PCR and immunofluorescence results both showed that orexin 1（OX,） and orexin 2（OX） receptors are presented in the LVN in *** brain slice preparations and whole-cell patch clamp recordings,a dose-dependent inward current elicited by orexin-A were observed in giant LVN neurons（diameter > 35μm,Deiters' neurons）.The orexin-A-elicited inward currents on the LVN neurons were not only partly blocked by selective OX,receptor antagonist SB334867 but also mimicked by selective OX receptor agonist[Ala,Z)-Leu]orexin -B,indicating that the orexin-A-induced excitation is mediated by both OX,an

关键词： orexin central orexmergic system lateral vestibular nucleus motor control cataplexy

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Orexin-A excites medial vestibular nucleus neurons through nonselective cation channels and Na+/Ca2+ exchangers

Orexin-A excites medial vestibular nucleus neurons through n...

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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： Xiao-Yang ZHANG,Qian-Xing ZHUANG,Jing-Ning ZHU~*,Jian-Jun WANG~* Department of Biological Science and Technology and State Key Laboratory of Pharmaceutical Biotechnology,School of Life Sciences,Mailbox 426,Nanjing University,22 Hankou Road,Nanjing 210093,China

Orexin is a newly discovered peptide which is synthesized exclusively within the lateral hypothalamic area and perifornical *** of orexin neurons causes narcolepsy-cataplexy,which is characterized by excessive daytime sleepiness,premature transitions to REM sleep,and sudden skeletal muscle weakness without impairment of ***,most studies so far on the pathogenesis of narcolepsy-cataplexy have been limited merely to the role of orexin in sleep-awake cycle,and the function of orexin on motor control has still been little *** the present study,effect of orexin-A on the medial vestibular nucleus（MVN）,which holds a key position in controlling head and eye movements,were *** histochemical results showed that both orexin 1 receptors（OX1Rs）and orexin 2 receptors（OX2Rs）are presented in the MVN in *** brain slice preparations and whole-cell patch clamp recordings,type-A and type-B MVN neurons were identified according to the shape of their after hyperpolarization action potentials.A dose-dependent increase in neuronal firing rates and an inward current elicited by orexin-A were observed in both type-A and type-B MVN *** orexin-A-elicited excitation on the type-A and type-B MVN neurons were not only partly blocked by selective OX1R antagonist SB334867 but also mimicked by selective OX2R agonist[Ala,Z)-Leu]-orexin B,indicating that the orexin-A-induced excitation on MVN neurons was mediated by both OX1R and ***,tetrodotoxin（TTX）did not block the excitations evoked by orexin-A,suggesting the actions of the peptide on MVN neurons are *** with an inward current elicited by orexin-A,a slight decrease of membrane conductance of the MVN neurons was observed and also was not blocked by TTX,suggesting activities of ion channels on postsynaptic membrane are increased by orexin *** I-V curves before and after application of orexin-A on MVN neurons showed that more than one ionic bas

关键词： orexin Orexin-A excites medial vestibular nucleus neurons through nonselective cation channels and Na exchangers

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Hydrogen sulfide suppresses sustained potassium channel currents of trigeminal ganglion neurons

Hydrogen sulfide suppresses sustained potassium channel curr...

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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： Xing-Mei FENG~1,You-Lang ZHOU~2,Fei-Hu QI~2,Ning-Ang LIU~3,Guang-Yin XU~(3,*) 1 Department of Stomatology(Department of Oral and Maxillofacial Surgery),Affiliated Hospital of Nantong University,Nantong 226001,China 2 Jiangsu Key Laboratory of Neuroregeneration,Nantong University,Nantong 226001,China 3 Institute of Neuroscience,Key Laboratory of Pain Research & Therapy,Soochow University,Suzhou 215123,China

Objective Hydrogen sulfide（HS）,an endogenous gaseotransmitter/modulator,is becoming appreciated that it may be involved in a wide variety of processes including inflammation and ***,the role and mechanism for HS in nociceptive processing in trigeminal ganglion（TG）neuron remains *** present study is to explore the role of HS on voltage-gated potassium channels and the distribution of endogenous HS synthyzing enzyme CBS expression in TG *** Whole cell patch clamp recordings were employed on acutely isolated TG neurons from adult male Sprague Dawley rats（6-8 week old）.Immunofluorescence studies were carried out to determine whether CBS was co-expressed in Kv1.1 or Kv1.4-positive TG *** In rat TG,（77.0±6.6）%neurons were immunoreactive for CBS,（85.1±3.8）%for Kvl.l and（97.8±1.1）%for Kv1.4. Double staining showed that all the CBS labeled cells were Kvl.l and Kvl.4 positive,but only（92.2±6.1）%of Kvl.l and（78.2±9.9）%of Kv1.4 positive cells contained CBS,*** of HS donor NaHS（250μM）led to a significant depolarization of resting membrane potential recorded from TG neurons（n=8,P<0.05）.Application of NaHS also resulted in a dramatic reduction in rheobase（P<0.05）,hyperpolarization of action potential threshold （P<0.05）,and a significant increase in the number of action potentials evoked at 2X and 3X rheobase stimulation （P<0.05）.Under voltage-clamp conditions,TG neurons exhibited transient A-type（I）and sustained outward rectifier K currents（I）.Application of NaHS did suppress the I density while did not change the I density of TG neurons （n=6）.Conclusion These data suggest that HS generated by endogenously expressed CBS in TG neurons increases neuronal excitability,which is largely mediated by suppressing I density,thus identifying for the first time a specific molecular mechanism underlying pain and sensitization in TG.

关键词： cystathionine-β-synthetase trigeminal ganglion voltage-gated potassium channels excitability

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Adeno-associated virus-mediated overexpression of netrin-1 attenuates ischemic brain injury in mice

Adeno-associated virus-mediated overexpression of netrin-1 a...

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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： Yong-Ting WANG~1,Hai-Yan LU~1,Jian-Rong LIU~2,Li-Li ZENG~2,Guo-Yuan YANG~(1,2,*) 1 Neuroscience and Neuroengineering Research Center,Med-X Research Institute,Shanghai Jiao Tong University, Shanghai 200030,China 2 Department of Neurology,Ruijin Hospital,School of Medicine,Shanghai Jiao Tong University,Shanghai 200025,China

Objective Netrin-1 is one of the axon-guiding molecules that are critical for neuronal development. Netrin-1 was found to stimulate the proliferation and migration of human cerebral endothelial cells in vitro and also promote focal neovascularization in normal adult mouse brain in *** the present study,we investigate the role of overexpression of netrin-1 via adeno-associated virus(AAV) mediated-gene transfer in a transient middle cerebral artery occlusion(tMCAO) model of *** We constructed adeno-associated virus carrying Netrin-1(AAVNT -1) or GFP gene(AAV-GFP,as a control).2.5μL of AAV-NT-1 suspension with 2×10～9 virus particles was injected stereotactically into the lateral ventricle of male CD-1 mice at a rate of 0.2μL/*** amount of AAV-GFP or saline was injected as controls(n=21 per group).Seven days after AAV-NT-1 injection,these mice underwent 60 min of tMCAO followed by 7 to 28 d of ***-1 expression was quantified by Western blot and Netrin-1 localization was determined by *** infarct volume and animal behavioral outcomes(beam walk test and Rotor-Rod test) were examined until the end of ***-stained microvessels were counted to determine the effect of Netrin-1 on angiogenesis after *** Endogenous Netrin-1 expression was induced in the ischemic penumbra of mouse brain by transient *** expression of Netrin-1 in the ischemic hemisphere was further enhanced after AAV-NT-1 gene *** neurons and astrocytes but not endothelial cells expressed Netrin-1 following AAV-NT-1 gene *** of Netrin-1 promoted the recovery of focal cerebra blood flow after MCAO in the AAV-NT-1-transduced mice compared to control group(P < 0.05).Brain infarct volume was decreased and neurobehavioral outcomes were greatly improved in the AAV-NT-1 transduced mice compared to the AAV-GFP or saline injected group of mice up to 28 days after tMCAO(P < 0.05).Microvessel counts were significantly i

关键词： adeno-asociated virus angiogenesis ischemia netrin-1 transient middle cerebral artery occlusion

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Cognitive impairment and expression of GFAP in diabetes rats and influence of insulin therapy

Cognitive impairment and expression of GFAP in diabetes rats...

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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： Yong-Zhong LIN~1,Yu JIAO~1,Min WU~1,Jin WANG~2,Chang-Kai SUN~(2,*) 1 Department of Neurology,The Second Affiliated Hospital of Dalian Medical University,Dalian 116027,China 2 Institution of Brain Disease of Dalian Medical University,Dalian 116027,China

Objective To investigate cognitive impairment and astrocytes reaction in diabetic rats and the influence of the insulin *** 52 health grown-up male Sprague-Dawley(SD) rats ware divided into 2 big groups stochastically:1-month group(n=26) and 3-month group(n=26);Each group then divided into 3 groups stochastically: diabetic group(n=10),insulin treatment group(n=10) and control group(n=6).Streptozotocin-induced diabetic model rat(60 mg/kg) was *** the insulin treatment group,the rats were treated with isophane insulin everyday(2-3 U/day) based on blood glucose *** of Morris water maze were taken place 1 month and 3 months later respectively,after which slices taken from hippocampus,basal ganglia,the white matter nearby lateral ventricle and frontal lobe were used to immunohistochemistral *** expression of GFAP positive cells was observed in diabetic ***(1) Spatial study and memory ability *** with control group,the swimming incubation period was prolonged in 3 month insulin treatment group(PO.05) and diabetic group including both 1-month(PO.05) and 3-month groups(PO.05),while that of 1-month insulin treatment group was not prolonged.(2) Compared with control group,the change of GFAP expression in different sites of brain was not significant in 1-month diabetic group and insulin treatment group including 1-month and 3-month *** in 3-month diabetic group the number of GFAP positive cells was more than control group in basal ganglia(P<0.05) and white matter nearby lateral ventricle (P<0.05).The number of GFAP positive cells in 3-month insulin treatment group was less than diabetic group in basal ganglia(P<0.05) and white matter nearby lateral ventricle(P<0.05).Conclusion(1) Diabetic rats present learning and memory dysfunction at 1st month.(2) The astrocytes change doesn't appear with early cognitive impairment in diabetic rats,suggesting cognitive impairment is not caused by astrocytes change.T

关键词： cognitive impairment diabetes GFAP insulin

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The effects of NMDAR and mGluR on Ap-mediated synaptic plasticity disruption in vitro

The effects of NMDAR and mGluR on Ap-mediated synaptic plast...

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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： Ru-Yi LIN,Tian-Xiang DENG,Gui-Lan LIU,Shu-Jun XU,Xaio-Wei CHEN,Xiao-Fei WEI,Qin-Wen WANG Medical School,Ningbo University,Ningbo 315211,China

Apart from anticholinesterases,memantine,a low-affinity NMDA receptor(NMDAR) antagonist,is the only currently approved treatment for clinical dementia of the Alzheimer *** we examined if subtype-preferring NMDA receptor antagonists could preferentially protect against the inhibition of NMDA receptor-dependent plasticity of excitatory synaptic transmission by Aβin the hippocampus by electrophysiology methods in *** selective for NMDA receptors containing NR2B but not NR2A subunits prevented Aβ-mediated inhibition of plasticity and showed *** AB,pretreatment with a high dose of NR2B antagonist ifenprodil(1μM) and Ro 25-6981(200 nM) completely inhibited *** experiments indicated that a lower dose of ifenprodil(400 nM) could partially block LTP(131±7%) and reverse Aβinhibition on LTP(139±6%).However,Ro 25-6981(50 nM) didn't block LTP(143±10%) but did prevent Aβinhibition on LTP(132±8%).The selective antagonist NVP-AAM077 for NMDA receptors containing NR2A did not affect LTP on its own,and failed to prevent the inhibition of LTP by Aβ.Furthermore,we also investigated LTD which was induced by strong LFS but not weak LFS,however,weak LFS plus Aβpresented a steady LTD in both the dentate gyrus and the CA1 region of the hippocampus.D-AP5(a specific NMDAR antagonist) could not block the LTD induced by Aβwith weak LFS in the CA1 *** contrary to the D-AP5,weak LFS with Aβ-induced LTD was completely abrogated by LY341495(the group I metabotropic glutamate receptor antagonist).Moreover,the enhancement of LTD by Ap was reversed by SB203580(p38 Mitogen-Activated Protein Kinase inhibitor) and phenylarsine oxide(membrane-permeable protein-tyrosine phosphatase inhibitor).The present data suggest that preferentially targeting NR2B subunit-containing NMDARs with a selective antagonist may provide an effective means of preventing cognitive deficits in Alzheimer's disease and LTD induced by Aβwith weak LFS was not NMDAR-dependent,but mGluR

关键词： Aβ AD synapse plasticity NMDA mGluR

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