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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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Spatial structure of neuronal receptive field in awake monkey secondary visual cortex(V2)

Spatial structure of neuronal receptive field in awake monke...

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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： Lu Liu Liang She Ming Chen Tianyi Liu Haidong Lu Yang Dan Mu-ming Poo Institute of Neuroscience State Key Laboratory of NeuroscienceCAS Center for Excellence in Brain ScienceShanghai Institutes for Biological SciencesChinese Academy of Sciences University of Chinese Academy of Sciences State Key Laboratory of Cognitive Neuroscience and Learning Beijing Normal University Division of Neurobiology Department of Molecular and Cell BiologyHoward Hughes Medical InstituteHelen Wills Neuroscience InstituteUniversity of California

Visual processing depends critically on the receptive field(RF) properties of visual neurons. However, comprehensive characterization of RFs beyond primary visual cortex(V1) remains a challenge. Here we report fine RF structures in secondary visual cortex(V2) of awake macaque monkeys, identified through a projection pursuit regression analysis of neuronal responses to natural images. We found that V2 RFs could be broadly classified as "V1-like"(typical Gabor-shaped subunits), "ultralong"(subunits with high aspect ratios), or "complex-shaped"(e.g., L- or T-junction-like subunits). Furthermore, single-unit recordings from functional domains identified by intrinsic optical imaging showed that neurons with ultralong RFs were primarily localized within pale stripes, whereas neurons with complex-shaped RFs were more concentrated in thin stripes. Thus, by combining single-unit recording with optical imaging and a novel computational approach, we have identified RF subunits underlying spatial feature selectivity of V2 neurons and demonstrated the functional organization of these RF properties.

关键词： receptive field,second visual cortex(V2),natural images,single-unit recording,opticalimaging of intrinsic signals

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Galectin-9 is increased during neuroinflammation and promotes remyelination

Galectin-9 is increased during neuroinflammation and promote...

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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： Steelman,A.J. Lu,H.C. Kim,S. Hernandez,J. Zhou,B. Li,J Laboratory of Immunophysiology and Behavior Department of Animal SciencesUniversity of Illinois Department of Veterinary Integrative Biosciences Texas A&M UniversityCollege Station

Objective Multiple sclerosis(MS) is an inflammatory and neurodegenerative disease of the central nervous system that causes substantial morbidity. Galectins are carbohydrate binding proteins that are capable of modulating immune responses. Galectin-9 is increased in the brains of MS patients, but its contribution to the natural history is unknown. Methods We utilized galectin-9 null(Lgals9-/-) mice to investigate the contribution of galectin-9 to inflammatory demyelination during experimental autoimmune encephalomyelitis(EAE) and cuprizone- and lysolecithin-induced de/remyelination. Results(1) Galectin-9 is increased in the CNS during EAE and cuprizone intoxication and localizes to macrophages/microglia and astrocytes.(2) Compared to control mice Lgals9-/-mice displayed heightened EAE severity which was associated with increased neuropathology and infiltration of MOG-specific Th17 cells.(3) Glial-derived galectin-9 did not influence the effector function or viability of Th17 cells in culture.(4) The absence of galectin-9 expression was associated with delayed remyelination.(5) Immunohistochemical analysis of the lesions revealed that Lgals9-/- mice have similar numbers of total(olig2+) oligodendrocytes, but a reduced number of mature(CC1+) oligodendrocytes compared to controls.(6) Treatment of primary mixed glial cultures with recombinant galectin-9 promoted oligodendrocyte maturation. Conclusion In response to inflammation galectin-9 becomes upregulated within the CNS, where it promotes repair.

关键词： Multiple sclerosis galectin-9 neuroinflammation EAE cuprizone remyelination

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Regulation of recurrent network activity by dopamine and norepinephrine in entorhinal cortical slices

Regulation of recurrent network activity by dopamine and nor...

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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： Ting He Yousheng Shu State Key Laboratory of Cognitive Neuroscience and Learning and IDG/McGovern Institute for Brain Research School of Brain and Cognitive SciencesBeijing Normal University

Cortical tissue is heavily innervated by neuropils containing neuromodulators such as dopamine(DA) and norepinephrine(NE). Release of these modulators can regulate brain states and higher order brain functions. It remains unclear how a specific neuromodulator regulates cortical states. In this study, we investigated the modulatory effect of DA and NE on the generation of cortical recurrent network activity- slow oscillations. We performed extracellular and whole-cell recording from entorhinal cortical slices that generated spontaneous slow oscillations, characterized as the occurrence of intermittent Up state(a period of depolarization with synaptic inputs) and Down state(a resting state of membrane potential with fewer synaptic inputs) in individual neurons. Light stimulation of the cortical tissue that expressed Ch R2 in tyrosine hydroxylase(TH)-expressing cells or neurites caused the generation of Up states and sometimes prolonged depolarization and firing followed by long-lasting hyperpolarization. Since TH-expressing fibers originating from midbrain can release DA or NE and modulate cortical states, we then delivered DA and NE through bath application and found surprisingly that both DA(10 and 50 M) and NE(10 and 100 M) completely abolished the occurrence of Up states. Close examination of slices obtained from entorhinal cortex revealed the existence of TH-expressing neurons with long apical dendrites extending towards the pia matter, suggesting that they could be glutamatergic cells and activation of these cells may trigger the generation of Up states. Together, our results from cortical slices suggest that the activation of local TH-expressing neurons triggers network activity, bath application of DA and NE, however, inhibits spontaneous network activity.

关键词： Slow oscillation,entorhinal cortex,dopamine,norepinephrine

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Location and orientation specificity in visual perceptual learning:Possible results of neural under-activations at untrained stimulus conditions

Location and orientation specificity in visual perceptual le...

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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： Cong Yu Department of Psychology IDG/McGovern Institute for Brain Researchand Peking-Tsinghua Center for Life SciencesPeking University

Training can improve a person's capability of discriminating fine stimulus differences in vision and other senses. This perceptual learning process has been one of the central topics in sensory neuroscience research because it reveals brain plasticity at a system level. For many years researchers on visual perceptual learning are excited by the observations of learning being specific to the trained retinal location and orientation, possible indications of neural plasticity in retinotopic and orientation selective early visual areas. Essentially all visual perceptual learning theories are either motivated or constrained by these specificities. However, previously we created new "double training" and "TPE" training paradigms to abolish these specificities and enable learning to transfer completely to untrained retinal locations and orientations. These demonstrations suggest that visualperceptual learning is a high-level learning process primarily occurring beyond the visual cortex. In the current study we examined why learning is specific to the trained location and orientation in the first place. In double training and TPE training, learning becomes transferable if the subjects are exposed to the untrained location or orientation through an irrelevant task, indicating that learning specificity may be to do with the untrained conditions. Here we used a continuous flash suppression technique, in which the perception of the stimulus presented to one eye is suppressed by flashing white noise presented to the other eye, to render the exposure stimuli subconscious. We then use additional stimulus manipulations to create "bottom-up only" stimulation and "top-down only" stimulation conditions. We found that bottom-up exposure of a grating stimulus at a untrained location or orthogonal orientation is sufficient to enable complete(location) or significant(orientation) learning transfer, while top-down influences without actual bottom-up stimulations may also enable(location) o

关键词： Perceptual learning specificity

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Erasure of recent and remote hippocampus-dependent fear memory by enhancing memory forgetting through increase in adult hippocampal neurogenesis

Erasure of recent and remote hippocampus-dependent fear memo...

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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： Satoshi KIDA Department of Bioscience Tokyo University of Agriculture

Erasure of fear memory is thought to be a therapeutic target for emotional disorders such as post-traumatic stress disorders. Memantine(MEM) is an N-methyl-D-aspartate glutamate receptor antagonist. Previous studies showed that MEM induced enhancement of adult hippocampal neurogenesis and memory forgetting formed recently. In this study, we tried to examine the effects of MEM treatment on forgetting of fear memory. Mice were contextual fear-conditioned with an electrical footshock(training) and then received systemic injections of MEM(50 mg/kg) once a week for 4 weeks. We found that MEM group displayed forgetting of contextual fear memory following the MEM treatment, while control group treated with VEH displayed normal contextual fear memory. Importantly, MEM group did not show spontaneous recovery of fear memory even a month after the MEM treatment. We next examined the relationship between forgetting of fear memory and increase in adult neurogenesis by MEM. After training, mice received injections of MEM followed by injections of 5-bromo-2-deoxyuridine(Brd U;50 mg/kg) 2 days later. Interestingly, there was a significant negative correlation between the number of Brd U-positive cells increased by MEM and differences of freezing scores before and after the MEM treatment. Moreover, MEM group displayed forgetting of hippocampus-dependent inhibitory avoidance memory, but not amygdala-dependent cued fear memory. These observations suggest that MEM treatment enables to erase hippocampus-dependent fear memory by enhancing memory forgetting through the increase in adult hippocampal neurogenesis. We are now examining effects of the MEM treatment on remote fear memory.

关键词： MEM Erasure of recent and remote hippocampus-dependent fear memory by enhancing memory forgetting through increase in adult hippocampal neurogenesis

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Angiotensin receptor blocker telmisartan promotes M2 microglia polarization

Angiotensin receptor blocker telmisartan promotes M2 microgl...

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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： Tao Pang Yuan Xu Ya-Zhou Xu Yun-Jie Wang Hong Liao Lu-Yong Zhang Jiangsu Key Laboratory of Drug Screening State Key Laboratory of Natural MedicinesChina Pharmaceutical University

Objective Brain inflammation plays an important role in the pathophysiology of many psychiatric and neurological diseases. Angiotensin II type 1 receptor blockers(ARBs) ameliorate brain inflammation and reduce M1 microglia activation. The ARB telmisartan suppresses neuroinflammation in cultured neuronal cells. We wished to clarify whether telmisartan prevents microglia-mediated neuroinflammation through microglia polarization to an anti-inflammatory M2 phenotype. Methods The gene expression of M1 markers and M2 markers was measured by RT-PCR. The AMPK phosphorylation level and M2 marker CD206 protein expression were determined by Western blotting. TNFα and IL-10 release was measured by ELISA. The gene knowdown was performed by the si RNA transfection experiment. Results Our results demonstrated that telmisartan promoted M2 polarization inLPS-stimulated BV2 and primary microglia cells. The promoting effects of telmisartan on M2 polarization were attenuated by an AMP-activated protein kinase(AMPK) inhibitor or AMPK knockdown, indicating that AMPK activation participates on telmisartan effects. Furthermore, telmisartan enhanced brain AMPK activation and M2 gene expression in a mouse model of LPS-induced neuroinflammation. Conclusion Our results indicate that telmisartan can be considered as a novel AMPK activator, suppressing neuroinflammation by promoting microglia M2 polarization. Telmisartan may provide a novel and safe therapeutic approach for the treatment of brain disorders associated with neuroinflammation.

关键词： Telmisartan Microglia polarization AMP-activated protein kinase Neuroinflammation

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Tmem108 regulates blood glucose level by interacting with PGM1

Tmem108 regulates blood glucose level by interacting with PG...

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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： Shun-Qi Wang Er-Kang Fei Jian-Dong Yu Xin-Sheng Lai Ming-Tao Xiong Hong-Yang Jing Bin Luo Peng Chen Min Yan Xi-Mo Dai Dong-Yan Ren Lin Mei The Laboratory of Synaptic Development and Plasticity Institute of Life ScienceNanchang University Department of Neuroscience and Regenerative Medicine Medical College of GeorgiaGeorgia Regents University

Tmem108(Transmembrane protein 108) mediates retrograde axonal transport in sensory neurons and regulates BDNF-triggered ERK signaling in CNS neurons. Recent GWAS(Genome-wide association study) discloses that it might have high correlation with heavy drinking, alcoholism and other substance addicts. In order to investigate its exact function in CNS, knockout Tmem108(KO Tmem108) mice are produced and cultured in our lab. Intriguingly, in our yeast two hybridized assay, we found that PGM1(Phosphoglucomutase 1) is one of the proteins which interact with intracellular domain of Tmem108. Furthermore, glucose level is being tested after fasting food 16 hours. Blood glucose level is higher in KO Tmem108 mice than in wild type mice after fasting food, and 3 hours later after intraperitoneal injection of glucose, blood glucose level is higher in wild type mice than in KO Tmem108 mice. We speculate that Tmem108 regulates blood glucose level by affecting PGM1 protein stability or enzyme activity, and that Tmem108 might involve in glucose metabolism dysfunction, such as diabetes.

关键词： Tmem108LRP4 blood glucose level,PGM1(Phosphoglucomutase 1)

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Optogenetic activation of anterior cingulate cortex inhibits the heroin seeking behavior in rats

Optogenetic activation of anterior cingulate cortex inhibits...

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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： Miaojun Lai Huaqiang Zhu Weisheng Chen Huifeng Liu Fuqiang Zhang Wenhua Zhou Laboratory of Behavioral Neuroscience Ningbo Addiction Research and Treatment CenterSchool of MedicineNingbo University

The aims of present study were to investigate effects of optogenetic activation of anterior cingulate cortex(ACC) on heroin self-administration, heroin seeking behavior induced by cues or heroin priming and learning and memory in rats. The rats in ACC optogenetic activation group were microinjected with 1μl pA AV-CaM KⅡα-hC hR 2-EYFP into ACC(AP:+2.7mm,ML:0.5mm,DV:2.5mm), then implanted optical fiber 0.5mm above site of microinjection. The rats in sham operation group were microinjected with AVV-EYFP into ACC. The rats were placed in operant chambers for a daily 4h heroin self-administration session under FR1 for consecutive 14 days. Then memory was taken eight-arms maze test. Optogenetic activation of ACC by illuminated by light(470 nm,5mW) decreased the enhancement of reference memory errors, working memory errors induced by heroin exposure. Moreover, optogenetic activation of ACC inhibited the heroin seeking behavior induced cues, which could be reversed partially by pretreatment with LY341495. While, Optogenetic activation of NAc core(AP:+1.2mm,ML:±3.2mm,DV:-6.7mm)also inhibited the heroin seeking induced by cues. In conclusion, these data demonstrate that activation of ACC can improve the cognitive dysfunction induced by heroin chronic exposure, and projective pathway from ACC to NAc core may be involved in the heroin seeking behavior induced by cues.

关键词： optogenetic cognitive fuction anterior cingulate cortex nucleus accumbens heroin metabotropic glutamate receptor

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Local mechanisms of acupoint stimulation:activation of cutaneous nerve fibers and mast cells

Local mechanisms of acupoint stimulation:activation of cutan...

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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： Jing-Jing CUI Mei-Ling Wu Dong-Sheng XU Long-Yan Yang Xiang-Hong JING Wan-Zhu BAI Institute of Acupuncture and Moxibustion China Academy of Chinese Medical Sciences

Nerve fibers and mast cells were considered to play a role in the action of acupuncture stimulation, however, their interaction remains unclear. In order to reveal the local mechanisms of acupoint stimulation, we focused our observation on the changes of cutaneous nerve fibers and mast cells under acupoint before and after needling. Acupoint Hegu(LI4) was selected as a representative target for acupuncture stimulation. The variations of nerve fibers and mast cells in the local area of LI4 with and without needling were performed by using immnohistochemistry, in which nerve fibers were examined with substance P(SP) and calcitonin gene-related peptide(CGRP), and mast cells examined with tryptase combining with histamine(HA) and serotonin(5-HT), respectively. After stimulation, most of mast cells gathered around the blood vessels and nerve fibers in the lower dermis and subcutaneous tissue under LI4. In addition, SP- and CGRP-positive labeling highly expressed on the local nerve fibers, and tryptase-, HA-, and 5-HT-positive labeling highly expressed on mast cells and granules. In contrast, SP- and CGRP-positive labeling was expressed lowly on the local nerve fibers and tryptase-, HA-, and 5-HT-positive labeling was also expressed lowly on a small number of intact mast cells in the normal control. These results indicate that local nerve fibers and mast cells under acupoints could be activated by acupuncture stimulation. As the neurotransmitters or neuromodulators, tryptase, HA, and 5-HT may play the active roles in transportation of acupuncture signals through the sensory pathway to the central nervous system.

关键词： LI4 calcitonin gene-related peptide substance P mast cell serotonin histamine manual acupuncture

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Allosteric modulating sigma-1 receptors elicits rapid anti-depressive activity

Allosteric modulating sigma-1 receptors elicits rapid anti-d...

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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： Yun Wang Lin Guo Huafeng Jiang Ao Zhang Xuechu Zhen Jiangsu Key laboratory for Translational Research for Neuropsychiatric diseases Department of PharmacologyCollege of Pharmaceutical SciencesSoochow University Department of Medicinal chemistry Shanghai Institute of Material MedicaChinese Academy of Sciences

Sigma-1 receptors are involved in the pathophysiological process of several neuropsychiatric diseases such as epilepsy, depression. Allosteric modulation represents an important mechanism for receptor functional regulation. In the present study, we examined anti-depressive activity of the latest identified novel and selective allosteric modulator of sigma-1 receptor SOMCL-668(3-methyl-phenyl-2, 3, 4, 5-tetrahydro-1H-benzo[d]azepin-7-ol). A single administration of SOMCL-668 decreased the immobility time in the forced swimming test and tailing suspended test in mice, which were abolished by pretreatment of sigma-1 receptor antagonist BD1047. In the chronic unpredicted mild stress(CUMS) model, chronic application of SOMCL-668 rapidly ameliorated anhedonia-like behavior(within a week), accompanying with the enhanced expression of brain-derived neurotrophic factor(BDNF) and phosphorylation of glycogen synthase kinase 3β(GSK 3β)(Ser-9). SOMCL-668 also rapidly promoted the phosphorylation of GSK 3β(Ser-9) in a allosteric manner in vitro. In the cultured primary neurons, SOMCL-668 enhanced the sigma-1 receptor agonist-induced neurite outgrowth and the secretion of BDNF. Taken together, SOMCL-668 is a potent and rapidly acting anti-depressive compound as a novel allosteric modulator of sigma-1 receptors. The present data provides the first evidence that allosteric modulation of sigma-1 receptor elicits a potent anti-depressive effect.

关键词： allosteric modulation anti-depressant sigma-1 receptor brain-derived neurotrophic factor glycogen synthase kinase 3β

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