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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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The role of V1 in visual stimulus contrast detection and external noise exclusion

The role of V1 in visual stimulus contrast detection and ext...

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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： Qian Wang Jin-Fang Yang Sang Jiang Cai-Hong Jin Rui-Long Liu Tian-Miao Hua College of Life Sciences Anhui Normal University

Objective Visual perception depends on the ability of visual system,especially the visual cortex, in detecting visual signals and excluding external noise. However, the relative contribution of different cortical areas to these functions remains unclear. This study tried to assess the role of primary visual cortex(V1) in the detection of stimulus contrast and exclusion of external noise added in the stimuli. Methods we trained 3 cats to discriminate between vertical and horizontal grating stimuli for conditioning training using 2-AFC method, and then measured the stimulus contrast threshold needed for cats to identify the visual stimuli masked by different level of external noise contrast(6 level: 0, 0.1, 0.2, 0.4, 0.6, 0.8), so as to construct psychophysical TvC(stimulus contrast threshold versus noise contrast) functions. Subsequently, We examined systematically the response of V1 neurons to different stimulus contrast under different levels of noise contrast using in vivo single-unit recording techniques. ROC(receiver operating characteristics) analysis was used to acquire the stimulus contrast threshold needed for V1 neurons to detect visual stimuli masked by different noise contrast, so as to build neuronal TvC functions. Results 1) The stimulus contrast threshold needed for 3 cats to identify visual stimuli increased with noise contrast levels added in the visual stimuli. 2) The stimulus contrast threshold needed for V1 neurons to detect visual stimuli also increased with noise levels in each cat. 3) At the low noise levels, the neuronal contrast threshold was quite close to psychophysical contrast threshold. However, with increasing noise, the neuronal contrast threshold was greatly higher than psychophysical one. Conclusion Neurons in V1 may play a major role in visual signal contrast detection, but contribute slightly to noise exclusion in visual signals.

关键词： Primary visual cortex,Visual stimuli,Contrast detection,External noise exclusion

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The peripheral and spinal mechanisms of bone cancer pain

The peripheral and spinal mechanisms of bone cancer pain

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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： Zhang Yu-Qiu Institute of Neurobiology Institutes of Brain Science and State Key Laboratory of Medical NeurobiologyCollaborative Innovation Center for Brain ScienceFudan University

Bone cancer-induced pain is one of the most severe types of chronic pain. Approximately 90% of advanced bone cancer patients must cope with chronic pain syndromes related to tumor progression and failed treatment. Transforming growth factor-β(TGF-β), a major bone-derived growth factor, is largely released by osteoclast bone resorption during the progression of bone cancer, which contributes to proliferation, angiogenesis, immunosuppression, invasion and metastasis. Here, we further pointed to that TGF-β1 is critical for the bone cancer-induced pain sensitization. We found that following the progression of bone cancer TGF-β1 was highly expressed in tumor-bearing bone, and its receptors, TGFβRI and TGFβRII, significantly increased in the dorsal root ganglia(DRG) in a rat model of bone cancer pain by intra-tibia inoculation of Walker 256 mammary gland carcinoma cells. Blockade of TGFβ receptors by TGFβRI antagonist SD-208 robustly suppressed bone cancer-induced thermal hyperalgesia on post-tumor day 14(PTD 14). Peripheral injection of TGF-β1 directly induced thermal hyperalgesia in intact rats and wide-type mice, but not in TRPV1-/- mice. Whole-cell patch-clamp recordings from DRG neurons showed that transient receptor potential vanilloid(TRPV1) sensitivity was significantly heightened on PTD14. Extracellular application of TGF-β1 significantly potentiated TRPV1 currents and increase of [Ca2+]i in DRG neurons. These findings suggest that TGF-β1 signaling contributes to bone cancer pain via the upregulation and sensitization of TRPV1 in primary sensory neurons, and therapeutic targeting of TGF-β1 may ease the bone cancer pain in advanced cancer. Accumulating evidence suggests that activation of spinal microglia contributes to the development of inflammatory and neuropathic pain. However, the role of spinal microglia in the maintenance of chronic pain remains controversial. In the present study, we demonstrated an unconventional role of spinal microglia in the maintenanc

关键词： TGF The peripheral and spinal mechanisms of bone cancer pain

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Impairment of TrkB Signaling in Angelman Syndrome and Targeted Intervention

Impairment of TrkB Signaling in Angelman Syndrome and Target...

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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： Zhiqing Zhang Suqing Yang Yuanyuan Liu Chuanlai Yang Nannan Chen Cong Cao Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases and Institute of Neuroscience Soochow University

Angelman syndrome(AS) is a severe autistic-like cognitive disorder caused by a deficient Ube3 A ubiquitin ligase. Neurological deficits have been linked to dysregulation of Ca2+/calmodulin-dependent protein kinase(Ca MKII) activity, resulting in impairment in long-term potentiation(LTP). Brain-derived neurotrophic factor(BDNF) is known to play a critical role in synaptic plasticity and memory. Our preliminary results found that the association of the PSD95(postsynaptic density protein PSD95)-Gαi proteins(inhibitory heterotrimeric G proteins α subunit) with Trk B is critical for intact BDNF *** AS mice, the BDNF-induced recruitment of PSD95, Gαi as well as PLCγ and Gab1 with Trk B receptors was attenuated, resulting in reduced activation of PLCγ-Ca MKII and PI3K-Akt. We characterized a bridged cyclic peptide(CN2097) shown by NMR studies to uniquely bind of PSD95 with high affinity, restored BDNF-induced Trk B/PSD95/Gαi complex formation, signaling and facilitated the induction of LTP in AS mice. We propose thatdefective BDNF signaling is the direct reason of Ca MKII abnormal, LTP loss and behavioral deficits in AS mice. The impaired association between PSD95 and Gαi might be responsible for Trk B signaling dysregulation in AS mice. The discovery that CN2097 can reinstate Trk B-signaling pathways in AS mice to facilitate LTP suggests that CN2097 might restore behavioral deficits in AS. We will also study the effects of CN2097 on postsynaptic AMPAR receptor content in the AS mice. Trk B-PSD95-Gαi signaling complex might be a beneficial drug target in treating the behavioral deficits in AS.

关键词： Angelman syndrome BDNF-TrkB signaling CaMKII PSD95 learning and memory

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Lesion of medulla's catecholaminergic neurons is associated with cardiovascular dysfunction in rotenone-induced Parkinson's disease rats

Lesion of medulla's catecholaminergic neurons is associated ...

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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： Zhaoqiang Zhang Xixun Du Huamin Xu Junxia Xie Hong Jiang Department of Physiology Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: PhysiologyShandong Provincial Collaborative Innovation Center for Neurodegenerative DisordersMedical College of Qingdao University Department of Physiology Basic Medical College of Taishan Medical University

Non-motor symptoms are of vital importance in Parkinson's disease(PD) in recent years, among which cardiovascular dysfunctions are commonly seen in PD patients before their motor signs. It is largely unknown the role of cardiovascular dysfunction in the progression of PD pathology and its underlying mechanisms. In the present study, in rotenone-induced PD rats, there was a gradual reduction in the number of nigral tyrosine hydroxylase-immunoreactive(TH-ir) neurons after 7, 14 and 21 days treatment. With the 56% reduction of striatal dopamine content and 52% loss of TH-ir neurons on 14 th day, the rats showed motor dysfunctions. However, normalized LF power(LFnu), low-frequency power(LF)/ high-frequency power(HF) ratio and mean blood pressure(MBP) reduction was observed as early as the 3rd day. Plasma norepinephrine(NE) and epinephrine(E) levels were decreased by 39% and 26% at the same time, respectively. Pearson's correlation analysis showed that either plasma NE or E levels positively correlated with MBP. Our results also showed that only the loss of catecholaminergic neurons in the rostral ventrolateral medulla(RVLM) emerged earlier than the nigral dopaminergic neurons, neither that of the caudal ventrolateral medulla(CVLM) nor the nucleus tractus solitarii(NTS). These suggest that dysfunction of catecholaminergic neurons in the RVLM might account for the reduced sympathetic activity, MBP and plasma catecholamine levels in the early stage of PD.

关键词： catecholaminergic neurons rostral ventrolateral medulla caudal ventrolateral medulla nucleus tractus solitarii Parkinson's disease

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Effects of creatine on BKCa channel in primary cultured rat cortical neurons deprivated of glucose

Effects of creatine on BKCa channel in primary cultured rat ...

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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： Chen Yao Tang Guangxu Lyu Yuanyuan Cai Jiajia Zhao Li Beijing Sport University Department of Physical Education Hexi University

Objective: Large-conductance Ca2+- and voltage-activated K+(BKCa) channels are expressed in almost every tissue in central nervous system and well known for their roles in regulation of membrane excitability. The importance of BKCa channels in determination of action potential duration and frequency, and neurotransmitter release has been demonstrated partly owing to their large conductance and to the synergic activation mechanism encompassing membrane depolarization and intracellular Ca2+/Mg2+. Glycogen could be a critical energy source for neurons activity including membrane excitability. When the glucose supply is inadequate(hypoglycaemia), the resultant hypoglycaemia may cause a decrease in neuronal membrane excitability. This study observed the effects of glucose deprivation and creatine pretreatment on BKCa in primary cultured rat cortical neurons. Method: The cultured neurons were randomized into control group(C), glucose deprivation group(GD) and CGD group which was deprived of glucose after 24-hour creatine pretreatment. Whole-cell patch-clamp techniques were used to record BKCa current. The changes of intracellular Ca2+concentration([Ca2+]i) were measured by using the fluorescent imaging via laser confocal scanning microscope. Results: *** current density of BKCa significantly increased after glucose deprivation for 2h but decreased after glucose deprivation for 4h(P<0.01) compared to those of C group. While pretreated with creatine, the current density of BKCa was much lower than those in the GD group after glucose deprivation for 2-3h(P<0.01). At the same time CGD group had no significantly changes ofcurrent density with the glucose deprivation time lasting. The comparison of half activation voltage and activation rate in all groups did not show any significant differences. 2. Based on fluorescence intensity measurement, GD group exhibited significantly increased in [Ca2+]i after glucose deprivation for 1-5h(P<0.01). Creatine pretreatment significantly

关键词： primary cultured rat cortical neurons glucose deprivation creatine BKCa channel

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A MRI study of methylene blue on ischemia/reperfusion-induced cerebral edema

A MRI study of methylene blue on ischemia/reperfusion-induce...

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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 Yan Qing Fang Zhong-Fang Shi Li-Xin Xu Li-Ping Dong Shao-Hua Yang Fang Yuan Department of Pathophysiology Beijing Neurosurgical InstituteBeijing Tiantan HospitalCapital Medical University Department of Pharmacology and Neuroscience University of North Texas Health Science Center

The neuroprotective effect of methylene blue has been proved by a number of studies for its unique functions as an alternative electron carrier, as well as energy-enhancing and antioxidant agent. In the current study, we evaluated the effects of MB on postischemic brain edema using MRI. Adult male rats(280 to 320 g) were subject to transient focal cerebral ischemia induced 1 h middle cerebral artery occlusion(MCAO), followed by reperfusion. MB was infused intravenously immediately after reperfusion and again at 3 h post-occlusion with the dosage of 3mg/kg and 1.5 mg/kg respectively. Normal saline was administered as vehicle control. Sequential MRI, including apparent diffusion coefficient(ADC) and T2-weighted Imaging(T2WI), were obtained at 0.5, 2.5 and 48 hours after the onset of stroke. In addition, final lesion volumes were analyzed by TTC staining at 48 h after stroke. Ischemic stroke induced ADC lesion volume at 0.5 h during MCAO which were temporal recovered at 1.5 h after reperfusion. No significant difference in ADC-defined lesion was observed between vehicle and MB treatment groups. At 48 h after stroke, MB significantly reduced ADC lesion and T2 WI lesion volume, attenuated cerebral swelling. Consistently, MB treatment significantly decreased TTC-defined lesion volume at 48 h after stroke. Taken together, this study demonstrated MB could decrease postischemic brain edema and provide additional evidence warrant future clinical investigation of MB for the treatment of ischemic stroke.

关键词： methylene blue stroke cerebral edema MRI

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Chinese Speech Decoding Using Intracranial EEG

Chinese Speech Decoding Using Intracranial EEG

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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： Bo Hong Department of Biomedical Engineering School of MedicineTsinghua University

A finite set of phonetic units is used in human speech, but how our brain recognizes these units from speech stream is still largely unknown. The revealing of this neural mechanism may lead to the development of new types of speech brain computer interfaces and computer speech recognition systems. In this study, we used intracranial EEG(iE EG) signal from human cortex to decode Chinese phonetic units during the perception of continuous speech. By exploring the time-frequency features, we identified i EEG electrodes that have selective response to specific Chinese phonemes. High-gamma power of these electrodes was further combined to separate sets of phonemes into clusters. The clustered organization largely coincided with phonological categories defined by discriminative features, similar as that has been found in English(Mesgarani et al, 2014). These findings were incorporated into a decoding framework of Chinese phonemes clusters and achieved consistent accuracies higher than chance level. Additionally, in tonal languages, like Chinese, lexical tone also serves as a key feature to provide contrast in word meaning. Behavior studies suggest that Mandarin Chinese tone is categorically perceived(Wang 1976;Xu et al. 2006). However, the neural mechanism underlying Mandarin tone perception is still poorly understood. In this study, an Oddball paradigm was designed by selecting two standard-deviant stimulus pairs with same physical distance but different category labels, among the synthesized tones with continuously varying pitch contours. Using i EEG recording over human auditory cortex, high temporal and spatial resolution cortical neural signals were used for the first time to investigate the cortical processing of lexical tone. We found distinct neural responses to the two standard-deviant tone pairs, and the difference increased from low to high-level electrodes along the hierarchy of auditory processing. In the two dimensional neural space, cross-category neural dis

关键词： Chinese Speech Decoding Using Intracranial EEG

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Resting-state functional connectivity between the dorsal anterior cingulate cortex and anterior insula/thalamus is associated with risky decision-making in nicotine addicts

Resting-state functional connectivity between the dorsal ant...

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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： Zhengde Wei Nannan Yang Lizhuang Yang Ying Wang Long Han Rujing Zha Ying Liu Peng Zhang Yifeng Zhou Xiaochu Zhang Key Laboratory of Brain Function and Disease Chinese Academy of SciencesSchool of Life SciencesUniversity of Science & Technology of China Provincial Hospital Affiliated to Anhui Medical University State Key Laboratory of Brain and Cognitive Science Institute of BiophysicsChinese Academy of Sciences School of Humanities & Social Science University of Science & Technology of China Center of Medical Physics and Technology Hefei Institutes of Physical ScienceCAS Centers for Biomedical Engineering University of Science & Technology of China

Nicotine addiction is associated with risky behaviors and with abnormalities in local brain areas related to risky decision making, including the dorsal anterior cingulate cortex(d ACC), anterior insula(AI), and thalamus. Although these brain abnormalities are anatomically separated, they may in fact belong to one neural network. Thus far, it is unclear whether circuit-level abnormalities lead to risky decision making in nicotine addicts. In the current study, we used task-based functional magnetic resonance imaging(f MRI) and examined the resting-state functional connectivity(RSFC) to study how connectivity between the d ACC, insula, and thalamus influence risky decision making in nicotine addicts. We found that an increase in risky decision making was associated with stronger nicotine dependence and stronger RSFC between the d ACC and right AI(rA I), the d ACC and thalamus, the d ACC and left AI(lA I), and the r AI and lA I, but the level of the risky decision making was not associated with risk level-related local activation. Furthermore, the severity of nicotine dependence was positively correlated with RSFC between the d ACC and r AI and between the d ACC and thalamus but was not associated with risk level-related local activation. Importantly, the d ACC-r AI and dA CC-thalamus couplings fully mediated the effect of nicotine-dependent severity on risky decision making. These results suggest that circuit-level connectivity may be a critical neural link between abnormally risky decision making and nicotine addiction.

关键词： decision making risky behavior nicotine addiction salience network fMRI RSFC

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Changes of dendritic spines and synapses in the process of brain development in APP/PS1 mice

Changes of dendritic spines and synapses in the process of b...

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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 Liu Yu-Juan Shi En-She Jiang Wen-Yi Yan Jin-Bo Deng Dong-Ming Yu Institute of Neurobiology Henan University Institute of Public Hygiene Henan University

Objective Alzheimer's disease(AD) is the most common form of dementia in elderly people. Synapse loss in AD animal models and patients exhibited a close correlation with cognitive deficits. However, the nature and progression of synaptic changes that lead to synapse dysfunction and loss remain to be fully characterized. The dendritic spine is the main structure in the formation of synapse, and its changes in structure and function were viewed as the marker of synaptic plasticity. The present study was to explore the sequence and causality between the age-dependent pathological changes of dendritic spines and synapses and the Aβ gradual accumulation in the brain development in APP/PS1 mice. Methods The hippocampus region of APP/PS1 mice from postnatal day 0 to postnatal day 360 were used as target section. DiI diotistic, immunohistochemistry, and transmission electron microscopy assays were applied to analyze the morphological changes of dendritic spines and synapses in brain tissue. Results(1) Amyloid plaques were observed from P6 m in APP/PS1 mice.(2) The length and density of dendritic spinesin CA1 area of APP/PS1 mice from P3 m were significantly lower than that in wild type mice respectively(P<0.05 and P<0.01).(3) Immunohistochemistrical results showed that the density of synaptophysin from P3 m were significantly reduced(P<0.01), and the synaptic ultrastructure also showed partly abnormalities in APP/PS1 mice. Conclusion The morphology of dendritic spines and synapses exhibited age-dependent changes in APP/PS1 mice and this change occurred earlier than the formation of Aβ plaques. Dendritic spine can be as a better target to evaluate the progress of AD.

关键词： Alzheimer's disease dendritic spine development Aβ hippocampus

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Research on the neuroprotective effects of CI-1206 in an APP/PS1 mouse model

Research on the neuroprotective effects of CI-1206 in an APP...

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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： Ju Yang Li Yuan Hui Shi Yu-Fei Han Xue-Song Qu Tian Li Juan-Juan Jiao Xue-Fan Dong Jin-Shun Qi Department of Physiology Shanxi Medical University

Objective Alzheimer disease(AD) is a fatal neurodegenerative disorder characterized by progressive cognitive impairment and memory loss. Type 2 diabetes mellitus has been identified as a risk factor for AD. Glucagon-like peptide 1(GLP-1), a natural gut hormone, not only modulated insulin signaling but also protected neuronal cells. Glucose-dependent insulinotropic polypeptide(GIP), an incretin hormone, normalizes insulin signaling and also acts as a neuroprotective growth factor. CI-1206, a single molecule that acts equally on the receptors for the GLP-1 and GIP, was recently demonstrated to be more effective in enhancing antihyperglycemic and insulinotropic efficacy relative to selective GLP-1 or GIP receptor mono-agonist in rodent models of obesity and diabetes. But it is not well known whether CI-1206 have some neuroprotective effects in APP/PS1 mouse model. Methods In this study we used morris water maze and electrophysiological recording techniques to analyze the neuroprotective effects of CI-1206 in an APP/PS1 mouse model. Results The behavioral study with Morris water maze showed a significant decline in spatial learning and memory of APP/PS1 mice, with an increased average escape latency in the hidden platform test and a decreased swimming time percent in the target quadrant in probe test, compared with the control group. But these performances were effectively reversed by CI-1206 treatment. In addition, CI-1206 prevented against suppression of hippocampal long term potentiation(LTP) induced by HFS. Conclusion The results demonstrate that CI-1206 protect the cognitive function and synaptic plasticity in APP/PS1 mouse model, suggesting that the GIP/GLP-1 receptor co-agonist might have the potential as a novel therapeutic agent for AD.

关键词： CI-1206 APP/PS1 mouse Morris water maze long term potentiation Alzheimer's disease

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