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检索条件"任意字段=第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议"

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Application of recombinant adeno-associate virus to cat V1

Application of recombinant adeno-associate virus to cat V1

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Hong-Liang Gong Li-Ling Qian Yi-Liang Lu Wei Wang Institute of Neuroscience State Key Laboratory of Neuroscience and Key Laboratory of Primate NeurobiologyShanghai Institutes for Biological SciencesChinese Academy of Sciences

The brain consists of many interconnected areas organized into complex networks. Accurately mapping of neuronal connectivity is fundamental for understanding how the brain processes information and generates behavior. Combined optogenetic techniques with recombinant adeno-associate virus(AAV) have emerged as a powerful tool for studying neural circuit structure and function particularly in mouse. However, little is known on the application of cat visual cortices, one of the best known vision models. In this study, we first injected AAV8-h Syn-GFP, AAV expressing green fluorescent protein under neuron-specific promoter, into primary visual cortex of cat. Histological analysis showed ahigh expression of GFP at the injection site and the fluorescent protein was expressed at neurons most located in layer 2/3, layer 5 and layer 6 of V1. The labeled projections from the injection site were well traced and terminated clearly at other visual areas such as d LGN and 21 a. To further explore the interplays among the labeled circuits, we employed two more AAV vectors expressing optogenetic fusion protein Ch R2-mcherry, AAV8-Ca MKIIa-Ch R2-mcherry and AAV8-h Syn-Ch R2-mcherry. We recorded robust spikes and LFP response following blue light stimulation at the injection site 4-5 weeks after injection. Together, our approach demonstrates that the combination of optogenetic tools and AAV offers great potential for circuit mapping and neural activity manipulating in cat visual system.

关键词： cat V1 adeno-associate virus optogenetics

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Simultaneous recording of decision making behavior and whole-brain neuronal activity of larval zebrafish

Simultaneous recording of decision making behavior and whole...

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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： Chun-Feng Shang Zhe Yang Chen Yang Yu-Fan Wang Sheng-Hao Li Ling-Feng Gou Jun Yan Ling Fu Jiu-Lin Du Institute of Neuroscience State Key Laboratory of NeuroscienceCenter for Excellence in Brain ScienceShanghai Institutes for Biological SciencesChinese Academy of Sciences Britton Chance Center for Biomedical Photonics Wuhan National Laboratory for OptoelectronicsHuazhong University of Science and Technology CAS-MPG Partner Institute for Computational Biology Shanghai Institutes of Biological Sciences

Struggling for survival and reproduction, animals need to extract salient information from superfluous sensory signals of various modalities and thus to make the right decision. While this process involves complex interaction among different brain areas, previous studies were mostly restrained to small populations of neurons in certain brain areas. Zebrafish is a relatively simple vertebrate animal model with a conserved brain architecture and rich repertoire of behaviors. With help of light-sheet illumination imaging, larval zebrafish offers an ideal preparation for studying multimodal-based decision-making. We have established a setup combining whole-brain imaging and behavior monitoring. Larval zebrafish at 6- 7 dpf were semi-restrained and presented with visual, auditory and olfactory stimuli. In fish with pan-neuronal expression of the Ca2+ sensor GCaM P5, we have evoked robust tail and eye movements and significant neuronal responses across large parts of the brain. In the next step, we will combine stimulation from different modalities, with congruent and incongruent ethological values, and examine the influence on behavior. With analysis of the embedded network structure and its dynamics in response to sensory stimuli with different valence, this work will shed light on the neural mechanisms underlying decision-making at a whole-brain scale.

关键词： zebrafish multisensory decision making light-sheet illumination imaging whole-brain behavior

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Real-time neurovascular imaging by laser speckle analysis-techniques,instrumentations and applications

Real-time neurovascular imaging by laser speckle analysis-te...

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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： Shanbao Tong Yao Li Hongyang Lu Hangdao Li School of Biomedical Engineering Med-X Research InstituteShanghai Jiao Tong University

Laser speckle imaging(LSI) has been used to obtain the 2-D profile of the blood flow and blood vasculature in real time, showing great potential of usefulness in neuroscience and neurology. We will introduce several high resolution of laser speckle imaging techniques that can be applied to monitor the neurovascular imaging in real time(1) High spatiotemporal LSI techniques by image processing and modeling. To solve the influences of the motion artifacts for in-vivo LSI, dark current and environmental artifacts due to the imaging system, and the estimation variances in blood flow speed, we proposed a registered laser speckle contrast analysis(rL ASCA) [1], enhanced laser speckle contrast analysis(e LASCA) [2] and random process estimation(RPE) of LASCA [3]. These techniques make it possible to have high resolution of blood flow velocity and vasculature information, and enable a real time blood flow imaging even for a freely moving animals.(2) Intraoperative neurovascular imaging by LSI. We developed several systems that facilitate real time neurovascular imaging during the neurologic surgery, which can be used for real time evaluation of the surgery [4] [5].(3) Neurovascular imaging for freely moving animals. Imaging the blood flow and neurovascular response when the animals are in a freely moving state has always been challenging. We will present a miniature head stage that can be mounted to the head of a rat for real time imaging [6]. Combining with multimodal optical techniques, we can even create and imagine a photothrombolic stroke model when the animal is in conscious and freely moving state [7]. The hemodynamic change can also be real time monitored [8] [9].

关键词： Laser speckle imaging,neurovascular imaging,brain injury,stroke

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Early single aspirin-triggered lipoxin blocked morphine anti-nociception tolerance through inhibiting NALP1 inflammasome:Involvement of PI3k/Akt signaling pathway

Early single aspirin-triggered lipoxin blocked morphine anti...

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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： Yu Tian Jun Wang Qian Li Yan-Qing Wang Department of Integrative Medicine and Neurobiology State Key Laboratory of Medical NeurobiologyFudan University

Clinical usage of opioids in pain relief is dampened by analgesic tolerance after chronic exposure, which is related to opioid-associated neuroinflammation. In the current study, based on chronic morphine tolerance rat model and sustained morphine treatment on primary neuron culture, it was observed that Akt phosphorylation, cleaved-Caspase-1-dependent NALP1 inflammasome activation and IL-1β maturation in spinal cord neurons were significantly enhanced by morphine. Moreover, treatment with LY294002, a specific inhibitor of PI3k/Akt signaling, significantly reduced Caspase-1 cleavage, NALP1 inflammasome activation and attenuated morphine tolerance. Tail-flick tests demonstrated that pharmacological inhibition on Caspase-1 activation or antagonizing IL-1β dramatically blocked the development of morphine tolerance. Intrathecal administration of Aspirin-triggered Lipoxin(ATL),an exogenous analogue of lipoxin, caused decline in Caspase-1 cleavage, inflammasome activation and mature IL-1β production and thus attenuated the development of morphine tolerance by inhibiting upstream Akt phosphorylation. Additionally, treatment with DAMGO, a selective μ-opioid receptor peptide, significantly induced Akt phosphorylation, Caspase-1 cleavage and anti-nociception tolerance, all of which were attenuated by ATL treatment. Taken together, the present study revealed the involvement of spinal NALP1 inflammasome activation in the development of morphine tolerance and the role of the μ-receptor/PI3k-Akt signaling/NALP1 inflammasome cascade in this process. By inhibiting this signaling cascade, ATL blocked the development of morphine tolerance.

关键词： morphine tolerance anti-nociception aspirin-triggered lipoxin(ATL) caspase-1 NALP1 inflammasome PI3k/Akt IL-1 spinal cord

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Chronic morphine treatment selectively regulates voltage-gated calcium channels in the rostral ventrolateral medulla of rats

Chronic morphine treatment selectively regulates voltage-gat...

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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： Ping Wang Jing Wang Zicheng Li Medical College of China Three Gorges University

Voltage-gated calcium channels are important targets for the treatment of allodynia. The rostral ventrolateral medulla(RVM) is closely related to allodynia. Chronic morphine treatment can induce allodynia. However, nothing has been known about whether morphine can induce allodynia by regulating Voltage-gated calcium channels in RVM. So we use western blot, PCR and patch clamp to study the effect of morphine on voltage-gated calcium channels. On one hand, we used the western blot and PCR methods to investigate the effect of morphine on the expression of voltage-gated calcium channels in RVM. Our results showed that chronic morphine treatment but not acute morphine treatment increased the expression of L-type calcium channels in RVM but not in prefrontal cortex and basolateral amygdala. Neither chronic morphine treatment nor acute morphine treatment regulated the expression of L-type calcium channels and T-type calcium channels in RVM, prefrontal cortex and basolateral amygdala. On the other hand, we used patch clamp to record Voltage-gated calcium channels currents. Our results indicated that chronic morphine treatment but not acute morphine treatment enhanced the peak currents of low-voltage operated calcium channels but not high- voltage operated calcium channels in RVM. Taken together, these results strongly imply chronic morphine treatment may induce allodynia by selectively regulating voltage-gated calcium channels in central nervous system.

关键词： morphine rostral ventrolateral medulla voltage-gated calcium channels

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Functional alterations in neurons of the auditory thalamus in tinnitus animal models

Functional alterations in neurons of the auditory thalamus i...

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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： Xin-Xing Wang Yan Jin Lin Chen Auditory Research Laboratory School of Life SciencesUniversity of Science and Technology of China

Our previous study shows that sodium salicylate(Na Sal), a tinnitus inducer, can hyperpolarize the membrane potential of neurons in rat medial geniculate body(MGB), a nucleus in the auditory thalamus(Su et al, 2012, PLoS ONE 7, e46969). The purpose of the present study was to investigate the underlying cellular mechanism. Whole-cell patch clamp recordings were made from horizontal brain slices containing the MGB of Wistar rats at P15—23. The change in the leak current was measured to represent that in the resting membrane potential when the mechanism of Na Sal-induced hyperpolarization was investigated. The rebound depolarization was recorded for assessing the effects of changes in the resting membrane potential on functional responses of MGB neurons. Na Sal could induce an outward leak current, indicating the drug can hyperpolarize MGB neurons. The current could be abolished by CGP55845, a GABAB receptor blocker, or by Ba2+ and Tertiapin-Q, blockers for G-protein-gated inwardly rectifying potassium(GIRK) channels, indicating that Na Sal hyperpolarizes the resting membrane potential by activating the GABAB-GIRK pathway. The Na Sal-induced hyperpolarization was shown to depress the rebound depolarization in MGB neurons. Our study demonstrates that NaS al targets GABAB receptors to hyperpolarize MGB neurons and alter their functional behaviors. The Na Sal-induced hyperpolarization is expected to change tonic firing to bursting firing in MGB neurons and serves as explanation for increased bursting firing and increased output of the MGB in Na Sal-induced tinnitus. Our findings favor the thalamocortical dysrhythmia hypothesis of tinnitus.

关键词： tinnitus auditory thalamus sodium salicylate GABAB-GIRK pathway

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Study of effects of GPR50 on synaptic plasticity and its mechanism

Study of effects of GPR50 on synaptic plasticity and its mec...

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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： Qi-Fa Li Bi-Ying Ge Chun-Yan Jiang Qiong Wu Xue-Fei Wu Yan Peng Jie Zhao Quan-Hong Ma Shao Li Department of Physiology Dalian Medical University Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases Institute of NeuroscienceSoochow University

GPR50(Orphan G protein-coupled receptor 50, GPR50) as a kind of G protein-coupled receptors(GGPCRs), has a similar structure namely the seven transmembraneα helices with other G protein-coupled receptors. Although its specific ligand is currently unknown, its distribution and function in the brain has a certain understanding. The expression of GPR50 has previously been found in the hippocampus, cortex, cerebellum, midbrain and other regions of brain. Its function is also reflected in its distribution characteristics and interaction with different molecules. LTP(Long-term potentiation) is activity-dependent enhancement in the efficacy of the synapses. It is a kind of synaptic plasticity and a wonderful model to understand the mechanism of learning and memory. NMDARs(N-Methyl-d-aspartate receptor) and GABAR(γ-Aminobutyric acid receptors) play an important role in the process of the occurrence and development of LTP. The main purpose of this study is to investigate the effects of GPR50 on synaptic plasticity and its possible mechanism. In our research, we found that GPR50 knockout mice showed deficit in synaptic plasticity. It demonstrated that excitatory postsynaptic potential slope and amplitude of GPR50 knockout mice are less than wild type mice(P<0.05). The protein expression level of NR2 B in hippocampus increased in GPR50 knockout mice. To the contrary, the protein expression level of GABAA receptor in hippocampus decreased in GPR50 knockout mice. The destruction of the balance of NMDAR and GABAR will lead to excitotoxicity. This may damage the synaptic plasticity.

关键词： GPR50 Learning and memory Excitotoxicity Synaptic plasticity

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Loss of Phenotype of Parvalbumin Interneurons Contrib utes to the Antidepressant Effects of Ketamine

Loss of Phenotype of Parvalbumin Interneurons Contrib utes 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： Guang-Fen Zhang Zhi-Qiang Zhou Xing-Ming Wang Wen-Xue Liu Jian-Jun Yang Department of Anesthesiology Jinling HospitalSchool of MedicineNanjing University

Depression is a highly prevalent disorder and currently available antidepressants have delayed onset of actions with low remission rates. Recent studies have confirmed that ketamine, a general anesthetic, exerts a rapid and robust antidepressant effect. The increased synaptic proteins and synaptic deconsolidation induced by mammalian target of rapamycin(m TOR) and glycogen synthase kinase-3(GSK-3) signal pathway play important roles in ketamine's antidepressant effect. The activation of glutamate-ergic NMDA receptors leads to the excitation of brain;whereas ketamine, as a NMDA receptor antagonist, also induces the excitation of the cerebral cortex. However, the mechanisms underlying this "paradoxical" phenomenon remain largely to be determined. Parvalbumin(PV) interneurons, as inhibitory interneurons, provide inhibitory signals to pyramidal *** previous studies have shown that ketamine reduces the expression of PV and glutamate decarboxylase 67(GAD67) in PV interneurons and increases the level of Glu in rats subjected to the forced swimming test. Inhibition of ketamine-induced loss of PV and GAD67 will block ketamine induction of antidepressant effects. Considering theses results, we raise a hypothesis that the dysfunction of PV interneurons results in the disinhibition of pyramidal cells, subsequently increases the Glu signal and activates the intracellular signals, which is an important mechanism underlying ketamine's antidepressant effect. Moreover, PV interneurons receive excitatory signals from pyramidal cells, and the interaction between these two kinds of cells plays a key role in the formation and regulation of γ oscillation neural microcircuit. In the near future, we will therefore apply electrophysiologic techniques to study the role of γ oscillation neural microcircuit mediated by PV interneurons in the antidepressant effect of ketamine and the underlying mechanisms.

关键词： Ketamine Antidepressant PV interneuron

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PGE2 modulates GABAA receptors via an EP1 receptor-mediated signaling pathway

PGE2 modulates GABAA receptors via an EP1 receptor-mediated ...

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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： Wen-Hao Dong Guang Yang Chang-Long Hu Yan-Ai Mei School of Life Sciences Institute of Brain Science and State Key Laboratory of Medical NeurobiologyFudan University

Objective PGE2 is one of the most abundant prostanoids in mammalian tissues, but its effect on neuronal receptors has not been well investigated. This study examines the effect of PGE2 on GABAA receptor currents in rat cerebellar granule neurons. Methods GABAA currents were recorded using a patch-clamp technique. Cell surface and total protein of GABAA ?1/2/3 subunits was carried out by Western blot analysis. Results Upon incubation of neurons with PGE2(1 ?M) for 60 minutes, GABAA currents were significantly potentiated. This PGE2-driven effect could be blocked by PKC or Ca MKII inhibitors as well as EP1 receptor antagonist, and mimicked by PMA or EP1 receptor agonist. Furthermore, Western blot data showed that PGE2 did not increase the total expression level of GABAA receptors, but significantly increased surface levels of GABAA ?1/2/3 subunits after 1 h of treatment. Consistently, both PKC and Ca MKII inhibitors were able to reduce PGE2-induced increases in cell surface expression of GABAA receptors. Conclusion Activation of either the PKC or Ca MKII pathways by EP1 receptors mediates the PGE2-induced increase in GABAA currents. This suggests that upregulation of postsynaptic GABAA receptors by PGE2 may have profound effects on cerebellar functioning under physiological and pathological conditions.

关键词： PGE2 GABAA receptors cerebellar granule cells EP receptor PKC

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Contribution of somatostatin- and parvalbumin-expressing interneurons to feature specific surround suppression in mouse V1

Contribution of somatostatin- and parvalbumin-expressing int...

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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： Fengling Li Haishan Yao Institute of Neuroscience and State Key Laboratory of Neuroscience Shanghai Institutes for Biological SciencesChinese Academy of Sciences University of Chinese Academy of Sciences

The responses of V1 neurons to stimuli in the receptive field(RF) can be modulated by stimuli outside the RF. The surround modulation often manifests as surround suppression, and the degree of suppression depends on the similarity between stimuli in the RF and the surround. Such feature specific surround suppression may underlie the perceptual phenomenon of figure-ground segregation. Recent studies demonstrated that specific types of inhibitory neurons in the visual cortex contribute to surround suppression of V1 neurons. However, the functional roles of specific interneuron types in the feature specific surround suppression remains unclear. In this study, by presenting preferred orientation in the RF and varying the orientation or phase of the surround grating, we examined how surround suppression depends on the difference in orientation or phase between RF and surround for V1 neurons in mice. More importantly, we used optogenetics technique to manipulate the activities of somatostatin- or parvalbumin-expressing interneurons and examined the effect on orientation tuning and phase tuning of surround suppression. We found that surround suppression in mouse V1 is both orientation-dependent and phase-dependent, with stronger suppression for iso-orientation surround or same-phase surround. The degree of orientation-specific surround suppression(OSSI) and phase-specific surround suppression(PSSI) are correlated. Suppressing the activity of somatostatin-expressing interneurons significantly reduced the surround suppression, consistent with previous reports. Our preliminary data also showed that SOM suppression did not significantly change PSSI or OSSI in anesthetized mice. We are now performing experiments to examine how activating specific interneuron types influences the orientation- or phase-dependent surround suppression.

关键词： feature specific surround suppression primary visual cortex(V1) inhibitory neurons mouse

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