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Protection effect of piperine and piperlonguminine from Piper longum *** against rotenone-induced neuronal injury

Protection effect of piperine and piperlonguminine from Pipe...

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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： Jia Liu Peng Zhang Hao Xing Hui Yang Center of Parkinson's Disease Beijing Institute for Brain Disorders Key Laboratory for Neurodegenerative Disease of the Ministry of EducationDepartment of Neurobiology Capital Medical University

Objective Parkinson disease(PD)is a chronic progressive disease which could involve multiple systems at its early stage while the central nervous system was finally injured at its later stage and manifested mainly as the movement disorder. Currently available treatment approaches for Parkinson's disease(PD) are limited and their efficacy was unsatisfactory. Reports showed that various symptoms including the medication wearing off and motor fluctuation will be emerged in PD patients after a mean time of 5 years of replacement treatment, and this bothers the patients a lot. Development of new drugs with better efficacy and less side effect urgently needed. Data proved that mitochondrial injured involved in the mechanism of PD and mitochondria could be potential target for the treatment of PD, our previous work found that alkaloids extraction from Piper longum L.(Piperaceae) had the capacity to resist Rotenone induced reactive oxygen species(ROS)and restore the mitochondrial membrane potential decrease. On the other hand data showed that mitochondrial permeability transition pore(mP TP) closely related to the function of mitochondria during its injury process. Reports proved that interfere the state of m PTP with its inhibitor could give rise to a protection effect. Based on our previous work, current study proved that alkaloids extraction from Piper longum L.(PLLE) exert its protection effect through inhibition of m PTP and stabilize the mitochondrial membrane potential and limit the apoptosis level induced by Rotenone injury. Method The rat was pretreatment with PLLE and ipsilateral intracranial infusion of rotenone was used to induce SNpc injury, protection effect of PLLE was analyzed through rotarod behavioral test, and western blot analysis to detect the tyrosine hydroxylase(TH)change in the mid-brain. Progressive Rotenone was also use to mimic the long lasting environment toxicity exposure and 7.0 Tesla MRI was used to get a dynamic change in the brain and catwal

关键词： Parkinson's disease treatment mitochondrial permeability transition pore

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Light stimulation into dorsal raphe nucleus contributes to antidepressant effect for stressed rats

Light stimulation into dorsal raphe nucleus contributes to a...

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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： Xiaotao Li Chaoran Ren Suk-yu Yau Endong Zhang Cheng Zhong Lu Huang Ting Zhang Mingliang Pu Gary E Pickard Kwok-Fai So The Brain Cognition and Brain Disease Institute for Collaboration Research of SIAT at CAS and the McGovern Institute at MIT Shenzhen Institutes of Advanced TechnologyChinese Academy of Sciences Department of Anatomy The University of Hong Kong Department of Ophthalmology The University of Hong Kong State key laboratory of Brain and Cognitive Science The University of Hong Kong Research Centre of Heart BrainHormone and Healthy AgingLi Ka Shing Faculty of MedicineThe University of Hong Kong GHM institute of CNS regeneration Jinan University Division of Medical Sciences UBC Island Medical ProgramUniversity of Victoria Department of Anatomy School of Basic Medical SciencesPeking University Key Laboratory on Machine Perception (Ministry of Education) Peking University Key Laboratory for Visual Impairment and Restoration (Ministry of Education) Peking University

Background: Cloudy weather without sunshine often makes people unhappy, while light therapy enables patients with depression symptoms to be remedied. However, the visual pathway underlying the light effect on mood remains unclear. Since a retino-raphe pathway was previously indicated to modulate 5-HT production, we hypothesize that the retinal projection into dorsal raphe nucleus(DRN) may play an important role in the light therapy for depression. Methods: We used a rat model of 14-day corticosterone administration(40 mg/kg/day subcutaneous injection) to test the effect of light therapy on non-seasonal depressant-like behavior, and the involved neural circuitry and neurochemistry as well. Results: Behavior results revealed that the bright light therapy, especially the blue light therapy with 470 nm and 400 lux, effectively reversed the depression-like responses in those stressed rats. After elimination of retino-raphe projection using immunotoxin(Saporin) the effect of light therapy was significantly attenuated. The activation of GABA cells with high c-Fos expression in the DRN involved in inducing an inhibition of 5-HT synthesis and a subsequent depressive behavior in the model with corticosterone administration. Whereas light therapy through retino-raphe projection deactivated the hyperaction of GABA cells inDRN, especially the 5-HT3 A positive GABA cells;that eventually contributed to the antidepressant effect from light therapy. Conclusions: Our results indicate that the retino-raphe circuitry contributed to the light therapy to the non-seasonal depression, and 5-HT3 A positive GABA cells in DRN was involved in mediating the function of retino-raphe projection.

关键词： depression dorsal raphe nucleus serotonin retinal projection light therapy GABA

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Mechanism of Long-Term Potentiation at Cerebellar Parallel Fiber-Purkinje Cell Synapses

Mechanism of Long-Term Potentiation at Cerebellar Parallel F...

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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： De-Juan Wang Li-Da Su Ya-Nan Wang Dong Yang Cheng-Long Sun Lin Zhou Xin-Xin Wang Ying Shen Department of Neurobiology Key Laboratory of Medical Neurobiology of the Ministry of HealthZhejiang Province Key Laboratory of NeurobiologyZhejiang University School of Medicine Neuroscience Care Unit Second Affiliated Hospital of Zhejiang University School of Medicine

Long-term depression(LTD) and long-term potentiation(LTP) at cerebellar parallel fiber-Purkinje cell(PF-PC) synapses play critical roles in motor learning. PF-PC synapses undergo two forms of LTP, which are expressed either presynaptically or postsynaptically depending on stimulus frequency. Upon PF stimulation at 4-8 Hz, presynaptically expressed LTP is evoked via presynaptic cyclic adenosine monophosphate signaling. The 1 Hz stimulation at PF-PC synapses induces a postsynaptically expressed LTP that requires a postsynaptic Ca2+ transient, phosphatases and nitric oxide(NO). However, the mechanism underlying 1Hz PF-LTP remains unclear because none of the known events is related to each other. Although lipid signaling is implicated in diverse biological functions, its importance in synaptic mechanisms has become increasingly evident. Here, we demonstrated that 1 Hz PF-LTP requires postsynaptic cytosolic phospholipase A2(c PLA2)/arachidonic acid(AA) signaling and presynaptic endocannabinoid receptors. Using patch-clamp recording in cerebellar slices, we found that 1 Hz PF-LTP was abolished in c PLA2-knock-out mice. This deficit was effectively rescued by the conjunction of 1 Hz PF stimulation and the local application of AA. 2-Arachidonoylglycerol(2-AG) and the retrograde activation of cannabinoid receptor 1(CB1R) were also involved in 1 Hz LTP because it was blocked by the hydrolysis of 2-AG or by inhibiting CB1 Rs. The amount of NO released was detected using an NO electrode in cultured granule cells and PF terminals. Our results showed that the activation of CB1 Rs at PF terminals activated NO synthetase and promoted NO production. The 1 Hz PF-stimuli evoked limited NO, but 100 Hz PF stimulation generated a large amount. Therefore, 1Hz PF-LTP, distinct from classical postsynaptically expressed plasticity, requires concurrent presynaptic and postsynaptic activity. In addition, NO of sufficient amplitude decides between the weakening and strengthening of PF-PC synaps

关键词： arachidonic acid cPLA2 endocannabinoids long-term potentiation parallel fiber Purkinje cell

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A novel mechanism of spine damages in stroke via DAPK1 and Tau

A novel mechanism of spine damages in stroke via DAPK1 and T...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Lei Pei Shan Wang Na Wei Honglin Yan Xin Yang Youming Lu Department of Neurobiology School of Basic MedicineHuazhong University of Science and Technology The Institute for Brain Research (IBR) Huazhong University of Science and Technology Department of Pathophysiology School of Basic MedicineHuazhong University of Science and Technology

Objective Loss of synaptic spine has been considered the earliest events of cerebral ischemia and generally assumed to be associated with the subsequent brain damages, but its underlying molecular mechanisms remain unknown. Our previous work demonstrated that DAPK1 in the postsynaptic domain phosphorylates NMDA receptor NR2 B at Serine-1303, eventually leading to neuronal death in stroke injury. Recently, we found that DAPK1 could also phosphorylate p53 at Serine-23 via direct binding of theDAPK1 death domain(DD) to the DNA-binding motif of p53(p53DM) in stroke in vitro. Though a handful of DAPK1 substrates have been identified, downstream signaling of DAPK1 that specifically mediates early spine damage after ischemic injuries is yet to be characterized. The present study aims to investigate whether the phosphorylation of Tau by DAPK1 induces spine damages in mouse models of focal cerebral ischemic stroke. Methods The interaction between DAPK1 and Tau was identified by co-immunoprecipition and glutathione S-transferase(GST) pull-down assay. The phosphorylation site was analyzed by mass spectrometry. Results(1)DAPK1 directly phosphorylates Tau on Serine-262(p S262) with it’s kinase domain(KD) and induces spine damage in stroke;(2)The binding domain of DAPK1 in the Tau microtubule repeat 1 domains has been identified as a sequence of IGSTENLK;(3)Genetic deletion of DAPK1 kinase domain(DAPK1-KD-/-) eliminates DAPK1-Tau interaction and substantially protects against synaptic spine damage following stroke onset;(4)Synthesized membrane permeable blocking peptide(TAT-R1D) disrupts DAPK1-Tau association and inhibits p S262;(5)Systematic administration of TAT-R1 D, 6 hours after stroke at a single dose of 2 mg/kg, produces therapeutic effects against stroke injuries. Conclusion Either genetic deletion of DAPK1 Kinase Domain or blocking DAPK1-Tau interaction by TAT-R1 D might be a promising strategy in clinical management of stroke.

关键词： DAPK1 dendritic spine stroke Tau phosphorylation therapeutics

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Sensory cortex neurons drive anticipatory motor responses

Sensory cortex neurons drive anticipatory motor responses

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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： Jingcheng Li Xiang Liao Jian Lu Ran Ding Meng Wang Xingyi Li Zhiqi Yang Jianxiong Zhang Yu Guang Hongbo Jia Shaoqun Zeng Zhian Hu Israel Nelken Xiaowei Chen Brain Research Center Third Military Medical University Department of Physiology Third Military Medical University Britton Chance Center for Biomedical Photonics Wuhan National Laboratory for OptoelectronicsHuazhong University of Science and Technology Brain Research Instrument Innovation Center Suzhou Institute of Biomedical Engineering and TechnologyChinese Academy of Sciences Department of Neurobiology Silberman Institute of Life Sciences and the Edmond and Lily Safra Center for Brain SciencesHebrew University CAS Center for Excellence in Brain Science Shanghai Institutes for Biological SciencesChinese Academy of Sciences

The ability of the brain to predict future events based on the pattern of recent sensory experience is critical for cognition, decision making, and motor actions1-4. For example, following rhythmic sensory stimulation that normally triggers the movement, animals often "over-react" by moving once or more at the expected time interval. In mammals, sensory neocortical circuits for immediate processing of sensory stimuli are well understood5-7, but whether and how these circuits may contribute to the anticipation of upcoming sensory stimuli remains unclear. Here we report the existence of ensemble neuronal activities in the mouse auditory cortex(ACx) that code for anticipation of the sound stimulus following rhythmic auditory stimulation. We show that such activity could drive anticipatory movement of the mice. Using in vivo two-photon Ca2+ imaging, we found that following a train of rhythmic sound stimulation, a subgroup of mouse layer(L) 2/3 and L5 ACx neurons exhibited one or a few repetitions of "echo" responses at the expected time interval in the absence of sound. These echo responses occurred preferentially at sound stimulus frequency that matched the best tuned frequency of the neuron. After learning to perform a sound-triggered licking task, mice showed "echo licking" responses following rhythmic sound stimulation that were highly correlated with ACx neuronal echo responses. Optogenetic activation8,9 of L5 ACx neurons, which provide the major ACx output, could substitute sound stimulation and reliably produce echo licking responses. Thus, anticipation of sound stimulus immediately following rhythmic sound stimulation is reflected by correlated activities of ACx neuronal ensembles, which are capable of driving anticipatory motor behavior

关键词： echo response anticipatory behavior auditory cortex circuit frequency selectivity two-photon

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Identification of specific targets of a command-like interneuron reveals novel roles of pattern-generating interneurons in Aplysia feeding network

Identification of specific targets of a command-like interne...

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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： Song-An Chen Ting-Ting Chen Ke Yu Dan-Dan Liu Ferdinand S Vilim Elizabeth C Cropper Klaudiusz R Weiss Jian Jing State Key Laboratory of Pharmaceutical Biotechnology Nanjing Advanced Institute for Life SciencesNanjing University School of Life Sciences Department of Neuroscience and Friedman Brain Institute Icahn School of Medicine at Mount Sinai

Activity of multifunctional networks is commonly initiated and modulated by a population of higher-order interneurons. In Aplysia the cerebral ganglion is essential for the feeding behavior. This has motivated efforts to identify and characterize cerebral higher order interneurons that project to the buccal ganglion, where the pattern generator is located. Backfill studies have determined that there are approximately 13 cerebral buccal interneurons(Xin et al 1999). Most of these cells have been studied, at least to some extent. For example, cerebral buccal interneuron 2(CBI-2) has been particularly well characterized. One CBI that has not been extensively investigated however is the neuron CBI-10. CBI-10 is located on the dorsal surface of the cerebral ganglion. Similar to CBI-2, CBI-10 is command-like, i.e., when it is stimulated buccal motor programs are triggered. The ability of CBI-10 to trigger motor programs is however weak. CBI-10 is like CBI-2 in that it contains the peptide CP-2 and it can drive both ingestive and egestive motor programs. We characterized synaptic connections between CBI-10 and buccal pattern-generating interneurons and found that CBI-10 elicits fast excitatory PSPs in buccal interneurons B34 and B40. The CBI-10-B34 connection is chemical and cholinergic, +2whereas the CBI-10-B40 connection is electrical, i.e., it persists in Ca- free saline. As expected B34 and B40 are both strongly active in motor programs elicited by CBI-10. Interestingly, hyperpolarization of either cell blocks the expression of CBI-10-elicited programs. This contrasts with CBI-2. Thus, although hyperpolarization of either B34 or B40 changes parametric features of CBI-2 induced activity, program expression is not blocked. In summary, we have characterized a novel command-like neuron that interacts with buccal pattern-generating interneurons in a unique manner. This increases the potential for diversity in motor program initiation, which may be important for meeting comp

关键词： Aplysia,feeding,command neurons,cholinergic

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Study of baicalin on sympathoexcitatory activity induced by myocardial ischemia via P2X2 receptor in rat superior cervical ganglia

Study of baicalin on sympathoexcitatory activity induced by ...

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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： Qiu-Lan Lv Shang-Dong Liang Li-Fang Zou Mo-Feng Ying Xi-Zhang Shou-Yu Wang Li-Li Guo Yun-Xue Shuang-Mei Liu Chang-Shui Xu Yun Gao Hong Xu Li-Chao Peng Miao-Miao Song Bing Wu Department of Physiology Medical School of Nanchang University

Objective Myocardial ischemia(MI) can induce myocardial tissues releasing large quantity of ATP, which activated P2X2 receptor in superior cervical ganglia(SCG) and made the SCG postganglionic neurons excited. Excitatory of sympathetic postganglionic efferent neurons increased the blood pressure and heart rates, which aggravated the myocardial ischemic injury. Although some studies had shown the protection of baicalin on myocardial ischemic injury. However, the precise mechanism is still unknown. Our study is to explore whether baicalin protects myocardium through inhibiting P2X2 receptor. Methods Blood pressure and heart rate were measured by non-invasive blood pressure meter with an indirect tail-cuff method. P2X2 receptor expression was tested by immunohistochemistry, Real-time RT- PCR and Western blotting. The concentration of serum CK-MB, c Tn-T, epinephrine and ATP was determine by biological reagent. Results(1) Baicalin can reduce the incremental concentration of serum CK-MB, cT n-T, epinephrine and ATP.(2) Baicalin decreased the up-regulated expression of P2X2 at both m RNA and protein in SCG, and then inhibited the sympathetic excitatory activity triggered by MI injury.(3) Baicalin can low blood pressure and heart rates obviously. Conclusion These results indicated that baicalin involved in the transmission of sympathetic excitation after the myocardial ischemic injury and might decrease sympathetic activity via inhibiting P2X2 receptor in rat SCG to protect myocardium.

关键词： P2X2 receptor sympathetic activity superior cervical ganglia baicalin

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Effects of aerobic exercise on CaMKⅡ in the central nervous system of APP/PS1 transgenic mice

Effects of aerobic exercise on CaMKⅡ in the central nervous...

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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： Lai-Kang Yu Bo-Ya Gu Li Zhao Department of Exercise Physiology Beijing Sport University

Objective Ca2+/calmodulin-dependent protein kinase Ⅱ(Ca MKⅡ) is the most abundant kinase within excitatory synapses in the mammalian brain. It interacts with and phosphorylates a large number of synaptic proteins to constitutively and/or activity-dependently regulate trafficking, subsynaptic localization, and function of the receptors. Numerous studies have shown that exercise is beneficial to learning and memory ability. This study aims to investigate the effects of 8 weeks aerobic exercise on the cognitive-behavior of APP/PS1 transgenic mice, synaptic numbers and the expression of Ca MKⅡα and P-Ca MKⅡαin cortex and hippocamp. Methods Thirty 4-month-old APP/PS1 transgenic mice were randomly divided into APP/PS1 sedentary group(AS) and APP/PS1 exercise group(AE), and fifteen 4-month-old C57BL/6J mice as the sedentary control(CS). The exercise groups mice participated in 8 weeks treadmill exercise,the speed was 15 m /min during the first 10 minutes,18 m /min during the following 50 minutes,and the slope was 0%. The behavioral change was detected by step-down fear conditioning, the cortical and hippocampal synaptic numbers were observed by transmission electron microscope(TEM), and the expression of Ca MKⅡα and P-Ca MKⅡα were measured by Western Blot. Results(1) AS mice behaviors and correct rates is lower than CS mice(P<0.05), while AE mice behaviors and correct rates is higher than those of AS mice(P<0.05).(2) Synaptic numbers of 6-month-old mice in cortex and hippocamp in AS is lower than that in CS(CA1 P<0.05;frontal lobe P<0.01), but it is higher in AE compared with AS(CA1 P<0.01;CA3 P<0.05;temporal lobe P<0.05;frontal lobe P<0.01) after 8 weeks aerobic exercise.(3) In hippocampal CA1 and CA3 regions, compared with the CS control group, the expression of Ca MKⅡα decreases significantly in AS(CA1 P < 0.01), while the expression of P-Ca MKⅡα shows a compensatory increase in AS;after 8 weeks aerobic exercise the expression of Ca MKⅡα in AE is obviously higher than t

关键词： aerobic exercise,Ca MKⅡ,synaptic loss,APP/PS1 transgenic mice

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Induction of spinal GluN2B-dependent LTP via BDNF contributes to the development of neuropathic pain

Induction of spinal GluN2B-dependent LTP via BDNF contribute...

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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： Xu Ding Wei Yang Hong Qin Huan-Min Wang Ke-Min Qi You Wan Guo-Gang Xing Beijing Pediatric Research Institute Beijing Children’s HospitalCapital Medical University Neuroscience Research Institute Peking University Department of Neurobiology School of Basic Medical SciencesPeking University Health Science Center

In previous studies, we have found that the Glu N2B-containing NMDA(NMDA-Glu N2B) receptors-mediated long-term potentiation(LTP) in the spinal cord play an important role in the development of central sensitization and neuropathic pain. Furthermore, we discovered that the brain-drived neurotrophic factor(BDNF) was likely the upstream signaling molecule for the activation of NMDA-Glu N2 B receptors. Recently, we investigated the signalling pathway for the activation of NMDA-Glu N2 B receptors by the spinal BDNF and to clarify its role in the development of neuropathic pain. We revealed that BDNF induces spinal LTP at C-fiber synapses via functional up-regulation of Glu N2B-NMDA receptors in the spinal dorsal horn, and this BDNF-mediated LTP-like state is responsible for the occlusion of spinal LTP elicited by subsequent highfrequency electrical stimulation(HFS) of the sciatic nerve in spinal nerve ligation(SNL) rats. We demonstrated that BDNF-evoked Src homology-2 domain-containing protein tyrosine phosphatase 2(SHP2) phosphorylation is required for subsequent Glu N2B-NMDA receptors up-regulation and spinal LTP induction, and also for pain allodynia development. Blockade of SHP2 phosphorylation in the spinal dorsal horn using NSC-87877 or SHP2 si RNA, not only prevents BDNF-mediated GluN 2B-NMDA receptors activation as well as spinal LTP induction and pain allodynia elicitation in intact rats, but also reduces the SNL-evoked Glu N2B-NMDA receptors up-regulation and spinal LTP occlusion, and ultimately alleviates pain allodynia in neuropathic rats. Taken together, our recent results suggest that the BDNF/SHP2/Glu N2B-NMDA signaling cascade plays a vital role in the development of central sensitization and neuropathic pain after peripheral nerve injury.

关键词： Brain-derived neurotrophic factor,SHP2,GluN2B-containing NMDA receptor,Long-term potentiation,Neuropathic pain,Spinal dorsal horn

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Peripheral nerve defect repair with PLGA conduit containing self-assembling peptide and peripheral blood derived mesenchymal stem cells

Peripheral nerve defect repair with PLGA conduit containing ...

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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： Xiang-Hai Wang Meng-Jie Pan Yi-Jing Chen Jin-Kun Wen Chang-Hui Qian Li-Xia Li Yuan-Yuan Li Jia-Song Guo Department of Histology and Embryology Southern Medical University Key Laboratory of Tissue Construction and Detection of Guangdong Province

Peripheral nerve injury(PNI) is one of the most common clinical diseases, and about half of PNI resulted in extensive nerve gaps which have to be reconstructed with nerve graft. Due to the shortage of natural nerve graft, fabricating ideal artificial nerve grafts has been widely accepted as a prospective strategy to repair the peripheral nerve defect. Recently, we reported a novel artificial nerve graft which is made of an outer porous poly(lactic-co-glycolic acid)(PLGA) conduit and an internal Self-assembling peptide(SAP) nanofiber scaffold. This graft had be used to bridge a 10 mm defect in rat sciatic nerve and got positive outcomes in functional recovery, axonal regeneration and remyelination. However, it still showed lower efficient than natural nerve graft. In order to improve the repair effects, we herein seeded peripheral blood derived mesenchymal stem cells(PBMSCs) into the inner scaffold of SAP before transplantation. 16 weeks after transplantation, motor function, nerve conduction, neuronal survival, axonal regeneration and remyelination, target muscle atrophy and re-innervation were assessed and compared with subjects treated with natural nerve graft, PLGA conduit with SAP, and empty PLGA conduit. Our results showed that, PBMSCs have mesenchymal stem cell's characters of immunophenotyping and multidifferentiation. Its can be induced into Schwann cells both in vitro and in vivo. Working as seed cells, PBMSCs significantly enhanced axonal regeneration and remyelination in the artificial nerve conduits, and some of PBMSCs contributed to form new myelin which were wrapping around regenerated axons. Moreover, PBMSCs improved the functional recoveries and alleviated the target muscle atrophy while compare to the groups of PLGA conduit with SAP and empty PLGA conduit. However, all aspects of morphologic and functional recoveries in the group of PLGA+SAP+PBMSCs still showed significant insufficient than that of natural nerve group. Taken together, our findings i

关键词： peripheral blood derived mesenchymal stem cells poly(lactic-co-glycolic acid)(PLGA) self assembling peptide artificial nerve graft neural regeneration peripheral nerve defect

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