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miR-181c-TRIM2 pathway is involved in cognitive deficiency induced by chronic cerebral ischemia/hypoxia

miR-181c-TRIM2 pathway is involved in cognitive deficiency 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： Chen Fang Liang Li Department of Pathology School of Basic Medical SciencesCapital Medical University

Objective Chronic cerebral ischemia is a serious threat to human health. Recent studies indicate particular mi RNA changes in response to ischemia/ hypoxia brain damage. However, little is known about the pattern of expression and the functions of these small RNA molecules in the pathogenesis of chronic cerebral ischemia. mi R-181 c is widely expressed in brain and closely related to the differentiation and development process of nervous system. The present study is to explore the effect of ischemia/hypoxia on the expression of mi R-181 c and its target ubiquitin ligase E3 TRIM2 in hippocampus. Methods The expression pattern of mi R-181 c in chronic cerebral ischemia was observed using 2-vessel occlusion(2VO) and oxygen-glucose deprivation(OGD) model. Bioinformatics and dual luciferase assay were established to validate TRIM2 as the target of mi R-181 *** manipulated levels of mi R-181 c using lentiviral vectors and mi R-181 c mimics. The influence of mi R-181 c to the cognitive capacity was examined by Morris water maze(MWM)task and step-through task. Results(1) Chronic cerebral ischemia led to the down regulation of mi R-181 c and high expression of TRIM2.(2) TRIM2 was the target gene of mi R-181 c which influenced the ubiquitination level of neurofilament light.(3) Over expression of miR-181 c in 2VO rats had protective effects on learning-memory dysfunction. Conclusion These data demonstrated that miR-181 c level changed in response to chronic cerebral ischemia in hippocampus. mi R-181 c might be involved in the cognitive impairment caused by ischemia/ hypoxia.

关键词： miR-181c TRIM2 ischemia/ hypoxia cognitive impairment

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Increased intracellular calcium is involved in lysosome mediated release of Amyloid-β in astrocytes

Increased intracellular calcium is involved in lysosome medi...

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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： Peng-yuan An Chen-xi Feng Yi-yi Zheng Meng-wei Xu Su-yan Shen Ning-xin Yu Xian-feng Chen Qing-wen Wang Shu-jun Xu Ningbo Key Laboratory of Behavioral Neuroscience Zhejiang Provincial Key Laboratory of PathophysiologySchool of MedicineNingbo University

Astrocytes have been considered playing a very important role in Altheimer's disease. Multiple signal molecules have been reported to be released from astrocytes that may mediate intercellular communications. It is well known that lysosome can degrade the endocytosed matter. However, whether lysosome can release Aβ under pathology stimulation and its underlying mechanism is unknown. In the present study, incubation of FM 1-43 for 2 h was used to label lysosome. Time lapse confocal microscope imaging was used to detect the changes of lysosome fluorescent. We found that fluorescence of FM1-43 was decreased under the constant stimulation of the ionomycin(1 μM) or glutamate(5 m M). This result indicated that astrocyte lysosome can exocytosis in Ca2+ dependent manner. On other side, we use the 488-labeled Aβ(500 n M) incubate astrocytes for 2h, and found out that Aβ were localized in lysosome. Moreover, the endocytosis Aβ can synchronize release synchoronize with lysosome. 1 μM ionomycin induce a destaining of 488-labeled-Aβ puncta to an extent(70%). It is significantly larger than that induced under the stimulation of the 5 m M glutamate(lower than 20%). These results indicated that differential modes of lysosome exocytosis Aβ may existed under different pathological stimulation. In addition, we also detect the medium content of Aβ outside astrocytes by ELISA. Our results showed that the content of Aβ in the medium increase significantly after ionomycin treatments. Taken together, our initial research shows astrocytes lysosome can release endocytosed Aβ in Ca2+ dependent manner. The study will provide better understanding of the pathogenesis of Alzheimer's disease, and will help us to find out new ideas and methods for therapeutic treatment of AD.

关键词： Altheimer's disease astrocyte lysosome exocytosis

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Neonatal exposure to sevoflurane induces long-term neuroendocrine abnormalities associated with repeated maternal separations in rats

Neonatal exposure to sevoflurane induces long-term neuroendo...

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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： Sijie Tan Anatoly E.Martynyuk Department of Histology and Embryology College of MedicineUniversity of South China Department of Anesthesiology University of Florida College of Medicine

Long-term developmental abnormalities are reported by animal studies and the majority of neurocognitive evaluations of children previously exposed to neonatal anesthesia. Whether neonatal anesthesia affects brain development only and what are underlying mechanisms remain to be determined. To address these questions, sevoflurane-induced long-term functional alterations in the brain and in the endocrine system and mechanistic roles of GABAAR-mediated excitation and increased corticosterone levels at the time of anesthesia in initiation of such alterations were investigated. The postnatal days 4, 5 or 6 Sprague-Dawley rats were anesthetized with 2.1% sevoflurane for 6 hrs;maternally separated and house reared only rats served as controls. The serum levels of corticosterone were measured immediately after anesthesia and in adulthood in response to stress. The hippocampal synaptic activity, behavior in elevated plus maze(EPM), and prepulse inhibition(PPI) of acoustic startle responses(sensorimotor gating function) were assessed in adulthood. Sevoflurane anesthesia markedly increased corticosterone levels in pups of both genders. In adulthood, these rats responded to stress with heightened secretion of corticosterone with greater increase in corticosterone levels in males versus females. Only male rats, previously exposed to neonatal sevoflurane, had higher frequency of miniature inhibitory postsynaptic currents in CA1 neurons, spent shorter time in open arms of the EPM and exhibited impaired PPI of startle. Pretreatment of male rats prior to sevoflurane with the NKCC1 inhibitor, bumetanide, or the corticosteroid receptor antagonist, RU28318, normalized endocrine responses to stress and EPM behavior in adulthood, while only those pretreated with bumetanide exhibited normalized PPI of startle responses. Neither bumetanide nor RU28318 altered the effect of sevoflurane on synaptic activity. In conclusion, neonatal sevoflurane induces endocrine and neurobehavioral abnormaliti

关键词： Sevoflurane HPA axis GABAAR,Neuroendocrine

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The effect and its potential mechanisms of STAT3 on synaptic plasticity in hippocampus of tmporal lobe epilepsy rats

The effect and its potential mechanisms of STAT3 on synaptic...

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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： Jin-Hai Gu Tao Sun Xin-Gang Li Gang Li Feng Wang He-Chun Xia Jian-Guo Niu Ningxia Key Laboratory of Craniocerebral Disease Ningxia Medical University Department of Neurosurgery General Hospital of Ningxia Medical University Department of Neurosurgery Qilu Hospital of Shandong University

Temporal lobe epilepsy(TLE) is the most common type of clinical refractory epilepsy, accounted for 60%. The patients with TLE could not be effectively controlled by long-term drug treatment. To study its pathogenesis and search for a better treatment method is very important. The main pathphysiological characteristic of TLE is mossy fiber sprouting(MFS) and subsequent synaptic reorganization in hippocampus, which may play an important role in the development and maintenance of epileptogenesis. The researcher think that MFS and subsequent synaptic reorganization make neurons form inappropriate synaptic connections and aberrant excitatory circuits in the process of epileptogensis, which increase the brain excitability,cause recurrent seizures,and contribute to the refractor epilepsy. What cellular and molecular events trigger MFS and synaptic reorganization is unresolved. The STAT3(signal transducer and activator of transcription 3), which controls the transcription activation of its downstream genes, is involved in the process of epileptogensis. However, there is little knowledge whether it involves in MFS of TLE. In this study,we firstly established the chronic TLE model kindled by electrical stimulation, and observed the expression of STAT3 and its phosphorylation protein in TLE models. Secondly the relationship between STAT3 pathway and MFS were observed by Timm staining and Western blot. Lastly,we investigate the potential mechanisms of STAT3 signaling pathway on synaptic plasticity in hippocampus of temporal lobe epilepsy. The results showed as follows:(1) The model was similar to the major characteristic of human TLE, so it could be used as ideal models in our study. Overexpression and constitutively activation of STAT3 are widely presented in hippocampus of the model;it suggests that aberrant STAT3 signaling pathway may play an important role in the pathogenesis of TLE.(2) MFS in hippocampus of TLE, which induced by seize, be inhibited by STAT3 signaling pathw

关键词： temporal lobe epilepsy signal transducers and activators of transcription 3 synaptic plasticity

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Glutamatergic projections from entorhinal cortex to dorsal dentate gyrus mediate context-induced reinstatement of heroin seeking

Glutamatergic projections from entorhinal cortex to dorsal 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： Feifei Ge Na Wang Cailian Cui Yijing Li Yan Liu Shuli Liu Haolin Zhang Xiaowei Sun Neuroscience Research Institute Peking University Department of Neurobiology School of Basic Medical SciencesPeking University The Ministry of Education the Ministry of Health

Objective Re-exposure to the context associated with heroin intake provokes relapse to drug in addicts after abstinence, in which the retrieval of drug-associated contextual memory is involved. Although both dorsal dentate gyrus(d DG) and entorhinal cortex(EC) play important role in contextual memory processing, little is known about their functions in contextual addiction memory. The present study is to explore whether the EC-d DG pathway mediates the context-induced reinstatement of heroin seeking. Methods Using self-administration(SA) rat model, neuronal activation and retrograde tracer were identified by immunofluorescence. The functions of the EC-d DG synaptic transmission was identified by electrophysiology in vivo in anaesthetized rats. Inactivation of the EC-d DG pathway was identified by chemogenetic strategy or disconnection procedure. The protein expression level in the d DG was identified by western blotting. Results(1) Neuronal activation and synaptic transmission in glutamatergic projections from the EC to d DG increased during context-induced reinstatement of heroin seeking.(2) Re-exposure to the heroin-paired context unregulated the phosphorylated Glu N2 B subunit-containing NMDA receptors(Glu N2B) at Y1472 and its downstream extracellular signal-regulated kinase(ERK1/2) in d DG region.(3) Inactivation of the EC-d DG pathway or the interaction of EC projecting to d DG local Glu N2B-ERK1/2 signaling both prevented the contextual heroin-seeking behavior, without influence on saccharin-reinforced responding or general locomotor activity. Conclusion The EC-d DG pathway mediates context-induced reinstatement of heroin seeking and that requires the activation of local postsynaptic Glu N2B-ERK1/2 signaling.

关键词： heroin context reinstatement dentate gyrus(dDG) entorhinal cortex(EC)

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Nicotine Exposure Recruits Glutamate Receptors to Postsynaptic Sites on Hippocampal Neurons in Culture

Nicotine Exposure Recruits Glutamate Receptors to Postsynapt...

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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 Duan Adrian F.Lozada Chen-yu Gou Jin Xu Yuan Chen Darwin K.Berg Department of Anatomy and Neurobiology Zhongshan School of Medicine Sun Yat-sen University Neurobiology Section Division of Biological Sciences University of California

Cholinergic neurons project throughout the nervous system and activate nicotinic receptors to modulate synaptic function in ways that shape higher order brain function. The acute effects of nicotinic signaling on long-term synaptic plasticity have been well-characterized. Less well understood is how chronic exposure to low levels of nicotine, such as those encountered by habitual smokers, can alter neural connections to promote addiction and other lasting behavioral effects. We show here that chronic exposure of hippocampal neurons in culture to low levels of nicotine recruits AMPA and NMDA receptors to the cell surface and sequesters them at postsynaptic sites. The receptors include Glu A2-containing AMPA receptors, which are responsible for most of the excitatory postsynaptic current mediated by AMPA receptors on the neurons, and include NMDA receptors containing NR1 and NR2 B subunits. Moreover, we find that the nicotine treatment also increases expression of the presynaptic component synapsin 1 and arranges it in puncta juxtaposed to the additional AMPA and NMDA receptor puncta, suggestive of increases in synaptic contacts. Consistent with increased synaptic input, we find that the nicotine treatment leads to an increase in the excitatory postsynaptic currents mediated by AMPA and NMDA receptors. Further, the increases skew the ratio of excitatory-to-inhibitory input the cell receives, and this holds both for pyramidal neurons and inhibitory neurons in the hippocampal CA1 region. The NR2B-containing NMDA receptor redistribution at synapses is associated with a significant increase in NR2 B phosphorylation at Tyr1472, a site known to prevent NR2 B endocytosis. These results suggest that chronic exposure to low levels of nicotine not only alters functional connections but also is likely to change excitability levels across networks. Further, it may increase the propensity for synaptic plasticity, given the increase in synaptic NMDA receptors.

关键词： Nicotine Nicotinic AMPA receptors NMDA receptors Hippocampus Glutamatergic Synapses

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Stereo processing in macaque visual area MT probed by graded anti-correlation of binocular stimuli

Stereo processing in macaque visual area MT probed by graded...

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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： Toshihide Yoshioka Takahiro Doi Mohammad Abdolrahmani Ichiro Fujita Grad Sch Front Biosci Osaka Univ Dept Neurosci Univ of Pennsylvania CiNet Osaka Univ and NICT

The visual system represents binocular disparity in correlation-based and match-based manners. In correlation-based representation, disparity is computed by the spatial cross-correlation between the left-eye and right-eye images. In match-based representation, disparity is computed only based on contrast-matched features between the two-eye images. We previously found that area V4, an intermediate stage along the ventral visual pathway, has the match-based representation of disparity at the population level. Here, we examined the disparity representation of the middle temporal(MT) area, a counterpart of V4 in the dorsal visual pathway. We recorded single unit activity of MT neurons from a monkey performing a fixation task. We manipulated random-dot stereograms(RDSs) with a graded anti-correlation technique(Doi et al., 2011) as we did in the previous V4 study. In this stimulus manipulation, the luminance contrast of varying proportion of random dots is reversed(from dark to bright and vice versa) in one eye image to dissociate the neuronal responses of the match-based and correlation-based representations. The RDSs consisted of a circular central patch and a surrounding annulus. Binocular disparity and the level of correlation(i.e., % of binocular correlation) were randomly changed from trial to trial for the center patch. The surrounding annulus always had zero disparity and 100% correlation. We refreshed dot-patterns of RDSs at 42.5Hz. The amplitude of disparity-tuning curve gradually decreased as the level of correlation was increased from 100%(normal RDSs) to 0%(RDSs with half of the dots contrast-reversed). Further correlation inverted the tuning-curve shapes and increased the tuning-curve amplitude. The tuning-curve amplitude at-100% correlation was significantly higher than that at 0% correlation. These changes of the disparity tuning functions at the single unit level agree with the correlation-based representation of disparity. We conclude that the disparity

关键词： binocular stereopsis neural representation binocular disparity tuning MT

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Affective circuits involving the prefrontal cortex:an optogenetic study in mice

Affective circuits involving the prefrontal cortex:an optoge...

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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 Yang Jun-ling Zhu Satoshi Ikemoto Guo-dong Gao Department of Neurosurgery Tangdu HospitalFourth Military Medical University Behavioral Neuroscience Branch National Institute on Drug AbuseNational Institutes of Health

The prefrontal cortex, known for executive cognitive functions such as planning and decision making, has also been implicated in affective functions. In particular, Brodmann's area 25 or the subgenual area of the human prefrontal cortex, which roughly corresponds to the dorsal peduncular cortex(DP) in rodent brain, has been an important target for treatment of clinical depression with deep brain stimulation. Although accumulating research supports efficacy of deep brain stimulation for mood disorders, little is known about brain circuits through which such manipulation alters affective state of patients. An optogenetic study was conducted in mice to examine possible circuits involved in affective function of the prefrontal cortex. C57BL/6J mice received adeno-associated viral vectors encoding the opsin channelrhodopsin-2(AAV-Ch R2) into one of prefrontal cortical areas, including the DP, intralimbic, prelimbic, medial orbital, lateral orbital, and premotor areas and adjacent olfactory cortices of the dorsal and ventral tenia tecta, and then optic fibers were implanted in these areas for subsequent photostimulation. To determine possible rewarding effect of the activation of local neurons, these mice were given the opportunity to press on a lever, an action that resulted in cortical stimulation with 8 light pulses(3 ms duration) delivered at the 25-Hz frequency. Each test session lasted 30 min, and sessions were repeated for 5 consecutive days. Mice quickly learned to self-stimulate neurons located in the medial part of the prefrontal cortex including the DP, intralimbic, prelimbic, medial orbital areas. By the 5th session, they responded over 1,000 times in 30 min. On the other hand, areas located in just dorsal, lateral or ventral to these medial areas did not support as vigorous self-stimulation behavior. To determine which brain regions mediate reward signals triggered by DP stimulation, the AAV-Ch R2 was injected into the DP, and optic fibers were implanted at o

关键词： Optogenetics,prefrontal cortex,self-stimulation,affective circuits

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The synaptic connections between CSF-Contacting Nucleus and brainstem descending inhibitory system,and the effects of CSF-Contacting Nucleus lesion on nociceptive behaviors

The synaptic connections between CSF-Contacting Nucleus and ...

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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： Siyuan Song Licai Zhang Jiangsu Province Key Laboratory of Anesthesiology Xuzhou Medical College

CSF-Contacting Nucleus was firstly labeled and termed by our research group in brain. The neuronal somas of CSF-Contacting Nucleus locate in brain parenchyma, and their processes stretch into cerebrospinal fluid. Therefore, it can be inferred that CSF-Contacting Nucleus might play a pivotal role in modulating both neuro-neural and neuro-humoral circuits. Our previous studies suggested that the CSF-Contacting Nucleus might play a pivotal role in pain modulation. The crosstalk of CSF-Contacting Nucleus with other sites in the brain mediating the pain modulation remains unknown. The CSF-Contacting Nucleus locates in the brainstem. The brainstem descending inhibitory system(PAG, DR, RVM, and LC), a widely accepted sites in pain modulation, also locates in the brainstem. In the present study, we observed the synaptic connections between CSF-Contacting Nucleus and brainstem descending inhibitory system. Furthermore, we observed the effects of CSF-Contacting Nucleus lesion on rats' nociceptive behaviors. Thus, we could demonstrate morphological pathways and behavior proofs of CSF-Contacting Nucleus in pain modulation. Rats received BDA, an anterograde tracer, microinjections into the CSF-Contacting Nucleus. The morphological connections towards the brainstem descending inhibitory system(PAG, DR, RVM, and LC) were observed under light microscopy, and the synaptic connections were confirmed under electron microscopy. Also, PAG, DR, RVM and LC received BDA microinjections respectively. The morphologicalconnections towards the CSF-Contacting Nucleus were observed under light microscopy, and the synaptic connections were confirmed under electron microscopy. Furthermore, rats received CB-SAP microinjection into the lateral ventricle to damage CSF-Contacting Nucleus specifically. The number of residual neurons in the CSF-Contacting Nucleus, as well as rats' nociceptive behaviors(MWT and PWL) was evaluated at day 0, 1, 3, 5, 7, 10 after lesion. The correlation between the number o

关键词： CSF-Contacting Nucleus descending inhibitory system tract-tracing study synaptic connection target-lesion pain

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The role of the dorsal prefrontal and posterior parietal cortexes in visual search using transcranial magnetic stimulation

The role of the dorsal prefrontal and posterior parietal cor...

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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-Long Yan Zhen-Lan Jin Ling Li Key Laboratory for Neuro Information of Ministry of Education School of Life Science and TechnologyUniversity of Electronic Science and Technology of China

Visual search for target requires many cognitive operations, including detecting the target, and inhibiting distractors. Although previously studies have shown that dorsal frontoparietal attentional network plays a crucial role in both bottom-up and top-down controls, the contribution of frontal cortex and parietal cortex to these processes remain elusive. Here we used repetitive transcranial magnetic stimulation(rT MS) to examine the functions of dorsal prefrontal cortex(DLPFC) and posterior parietal cortex(PPC) in a visual search task. Participants searched a target accompanied with three distractors which defined by color and orientation to create either "pop-out" or "search" conditions. In the "pop-out" condition, the color and orientation of the three distractors differed from that of the target. In the"search" condition, however, only the orientation of the distractors differed from that of the target. Event-related rT MS(10Hz, 100% motor threshold, 2 pulses) was applied to right DLPFC and PPC sites in different days. Performance, as measured by reaction times(RTs) and accuracy, was established at baseline(no r TMS), during r TMS, and after r TMS(Post-session). The RTs in search condition but not pop-out condition was delayed when rT MS was applied to DLPFC relative baseline session. On the other hand, r TMS over the PPC delayed the RTs only when target was presented in left visual field in both pop-out and search conditions. The baseline and Post-session did not have significant differences which further demonstrated the inhibiting effect of rT MS. These findings show that DLPFC and PPC play a crucial role in bottom-up and top-down processes. We suggest that inhibition of the right PPC by means of rT MS disturbs visual search in the contralateral visual field by inhibiting the spatial attentional processes.

关键词： Right dorsal prefrontal cortex right posterior parietal cortex rTMS visual search

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