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Short-Term Visual Experience Leads to potentiation of Spontaneous Activity in Mouse Superior Colliculus

Neuroscience Bulletin 2021年第3期37卷 353-368页

作者： Qingpeng Yu Hang Fu Gang Wang Jiayi Zhang Biao Yan Institutes of Brain Science State Key Laboratory of Medical Neurobiology and Ministry of Education Frontiers Center for Brain ScienceDepartment of OphthalmologyZhongshan HospitalFudan UniversityShanghai 200433China Center of Brain Sciences Beijing Institute of Basic Medical SciencesNo.27Taiping RoadHaidian DistrictBeijing 100850China

Spontaneous activity in the brain maintains an internal structured pattern that reflects the external environment,which is essential for processing information and developing perception and cognition.An essential prerequisite of spontaneous activity for perception is the ability to reverberate external information,such as by potentiation.Yet its role in the processing of potentiation in mouse superior colliculus(SC)neurons is less studied.Here,we used electrophysiological recording,optogenetics,and drug infusion methods to investigate the mechanism of potentiation in SC neurons.We found that visual experience potentiated SC neurons several minutes later in different developmental stages,and the similarity between spontaneous and visually-evoked activity increased with age.Before eye-opening,activation of retinal ganglion cells that expressed ChR2 also induced the potentiation of spontaneous activity in the mouse SC.potentiation was dependenton stimulus number and showed feature selectivity for direction and orientation.Optogenetic activation of parvalbumin neurons in the SC attenuated the potentiation induced by visual experience.Furthermore,potentiation in SC neurons was blocked by inhibiting the glutamate transporter GLT1.These results indicated that the potentiation induced by a visual stimulus might play a key role in shaping the internal representation of the environment,and serves as a carrier for short-term memory consolidation.

关键词： Spontaneous activity Visual experience potentiation Superior colliculus Feature selectivity Glutamate homeostasis

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Active fraction combination from Liuwei Dihuang decoction(LW-AFC) ameliorates corticosterone-induced long-term potentiation impairment in mice in vivo

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中国药理学与毒理学杂志 2019年第6期33卷 436-437页

作者： HUANG Yan LI Dong CHENG Bin LIU Gang ZHANG Yong-xiang ZHOU Wen-xia Beijing Institute of Pharmacology and Toxicology State Key Laboratory of Toxicology and Medical Countermeasures

Liuwei Dihuang decoction(LW), a classic formula in traditional Chinese medicine(TCM), has been used for nearly one thousand years for various diseases with characteristic features of kidney yin deficiency. LW consists of 6herbs including Dihuang[prepared root of Rehmannia glutinosa(Gaertn) DC], Shanyao(rhizome of Dioscorea polystachya Turcz), Shanzhuyu(fruit of Cornus officinalis Siebold Zucc), Mudanpi(root bark of Paeonia × suffruticosa Andrews),Zexie(rhizome of Alisma plantago-aquatica L) and Fuling(scleorotia of Wolfiporia extensa(Peck) Ginns)LW-active fraction combination(LW-AFC) is extracted from LW, it is effective for the treatment of kidney yin deficiency in many animal models. There are 3 fractions in LW-AFC, a polysaccharide fraction(LWB-B), a glycoside fraction(LWD-b) and an oligosaccharide fraction(CA-30). Our previous results indicate that LW-AFC has similar pharmacological effects to LW, modulating the balance of the NIM network. LW-AFC has positive effects in many animal models of kidney deficiency or disturbance of the NIM network. LW-AFC could improve the cognitive ability in Alzheimer′s disease(AD) animal models(APP/PS1, SAMP8), where modulating immune function and balancing the NIM network may play an important role in its cognition improving effects. Our study also showed that LW-AFC had protective effects on stress-induced disturbances of the NIM network. However, the underlying mechanisms remain elusive and need further investigation. OBJECTIVE This study evaluated the effects of LW-AFC and the active fractions(polysaccharide, LWB-B;glycoside, LWD-b;oligosaccharide,CA-30) on corticosterone(Cort)-induced long-term potentiation(LTP) impairment in vivo. METHODS LTP was used to evaluate the synaptic plasticity. LW-AFC was orally administered for seven days. The active fractions were given by either chronic administration(ig, ip, 7 d) or single administration(icv, ig, ip). Cort was injected subcutaneously 1 h before the high-frequency stimulation(HFS) to induce LTP impairment. Moreover, in order

关键词： LW-active fraction combination active fractions corticosterone long-term potentiation synaptic plasticity stress

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Parishin C's prevention of Aβ_(1–42)-induced inhibition of long-term potentiation is related to NMDA receptors

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Acta Pharmaceutica Sinica B 2016年第3期6卷 189-197页

作者： Zhihui Liu Weiping Wang Nan Feng Ling Wang Jiangong Shi Xiaoliang Wang State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Institute of Materia MedicaChinese Academy of Medical Sciences & Peking Union Medical College

The rhizome of Gastrodia elata(GE), a herb medicine, has been used for treatment of neuronal disorders in Eastern Asia for hundreds of years. Parishin C is a major ingredient of GE. In this study, the i.c.v. injection of soluble Aβ1–42oligomers model of LTP injury was used. We investigated the effects of parishin C on the improvement of LTP in soluble Aβ1–42oligomer–injected rats and the underlying electrophysiological mechanisms. Parishin C(i.p. or i.c.v.) significantly ameliorated LTP impairment induced by i.c.v. injection of soluble Aβ1–42oligomers. In cultured hippocampal neurons,soluble Aβ1–42oligomers significantly inhibited NMDAR currents while not affecting AMPAR currents and voltage-dependent currents. Pretreatment with parishin C protected NMDA receptor currents from the damage induced by Aβ. In summary, parishin C improved LTP deficits induced by soluble Aβ1–42oligomers. The protection by parishin C against Aβ-induced LTP damage might be related to NMDA receptors.

关键词： Parishin C Long-term potentiation Neuroprotection NMDA receptors Ion channels

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Glutamate receptor delocalization in postsynaptic membrane and reduced hippocampal synaptic plasticity in the early stage of Alzheimer's disease

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Neural Regeneration Research 2019年第6期14卷 1037-1045页

作者： Ning Li Yang Li Li-Juan Li Ke Zhu Yan Zheng Xiao-Min Wang Department of Neurobiology Capital Medical University Key Laboratory for Neurodegenerative Disorders of the Ministry of Education Capital Medical University Beijing Institute for Brain Disorders Department of Physiology Capital Medical University

Mounting evidence suggests that synaptic plasticity provides the cellular biological basis of learning and memory, and plasticity deficits play a key role in dementia caused by Alzheimer's disease. However, the mechanisms by which synaptic dysfunction contributes to the pathogenesis of Alzheimer's disease remain unclear. In the present study, Alzheimer's disease transgenic mice were used to determine the relationship between decreased hippocampal synaptic plasticity and pathological changes and cognitive-behavioral deterioration, as well as possible mechanisms underlying decreased synaptic plasticity in the early stages of Alzheimer's disease-like diseases. APP/PS1 double transgenic(5 XFAD; Jackson Laboratory) mice and their littermates(wild-type, controls) were used in this study. Additional 6-weekold and 10-week-old 5 XFAD mice and wild-type mice were used for electrophysiological recording of hippocampal dentate gyrus. For10-week-old 5 XFAD mice and wild-type mice, the left hippocampus was used for electrophysiological recording, and the right hippocampus was used for biochemical experiments or immunohistochemical staining to observe synaptophysin levels and amyloid beta deposition levels. The results revealed that, compared with wild-type mice, 6-week-old 5 XFAD mice exhibited unaltered long-term potentiation in the hippocampal dentate gyrus. Another set of 5 XFAD mice began to show attenuation at the age of 10 weeks, and a large quantity of amyloid beta protein was accumulated in hippocampal cells. The location of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor and N-methyl-D-aspartic acid receptor subunits in synaptosomes was decreased. These findings indicate that the delocalization of postsynaptic glutamate receptors and an associated decline in synaptic plasticity may be key mechanisms in the early onset of Alzheimer's disease. The use and care of animals were in strict accordance with the ethical standards of the Animal Ethics Committee of Capital Medical University,China on December 17, 2

关键词： nerve regeneration Alzheimer’s disease synaptic plasticity hippocampus learning and memory long-term potentiation βamyloid glutamate receptor synaptic strength neural regeneration

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Mechanisms by which fibroblast growth factor 20 improves motor performance in a mouse model of Parkinson’s disease

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Neural Regeneration Research 2019年第8期14卷 1438-1444页

作者： Ai-Qin Wang Li-Na Kong Ming-Zhu Meng Xiu-He Zhao Si Chen Xiao-Tang Wang Qilu Hospital of Shandong University

Genome-wide studies have reported that Parkinson's disease is associated with abnormal expression of various growth factors. In this study, male C57BL/6 mice aged 10 weeks were used to establish Parkinson's disease models using an intraperitoneal injection of 60 mg/kg 1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine. 28 days later, 10 or 100 ng fibroblast growth factor 20 was injected intracerebroventricularly. The electrophysiological changes in the mouse hippocampus were recorded using a full-cell patch clamp. Expression of Kv4.2 in the substantia nigra was analyzed using a western blot assay. Serum malondialdehyde levels were analyzed by enzyme-linked immunosorbent assay. The motor coordination of mice was evaluated using the rotarod test. The results showed that fibroblast growth factor 20 decreased A-type potassium current in neurons of the substantia nigra, increased long-term potentiation amplitude in the hippocampus, and downregulated Kv4.2 expression. A high dose of fibroblast growth factor 20 reduced serum malondialdehyde levels and enhanced the motor coordination of mice. These findings confirm that fibroblast growth factor 20 has a therapeutic effect on the toxicity induced by l-methyl-4-phenyl-l,2,3s6-tetrahydropyridine, and its mechanism of action is associated with the inhibition of A-type K^+ currents and Kv4.2 expression. All animal procedures were approved by the Animal Care and Use Committee of Qilu Hospital of Shandong University, China in 2017 (approval No. KYLL-2017-0012).

关键词： nerve regeneration Parkinson's disease l-methyl-4-phenyl-1,2,3,6-tetrahydropyridine fibroblast growth factor 20 A-type potassium current long-term potentiation Kv4.2 oxidative stress malondialdehyde motor performance neural regeneration

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Paired associative stimulation improves synaptic plasticity and functional outcomes after cerebral ischemia

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Neural Regeneration Research 2019年第11期14卷 1968-1976页

作者： Yan Hu Tie-Cheng Guo Xiang-Yu Zhang Jun Tian Yin-Shan Lu Department of Rehabilitation Medicine Tongji HospitalTongji Medical CollegeHuazhong University of Science & TechnologyWuhanHubei ProvinceChina Department of Rehabilitation Medicine Zhongnan Hospital of Wuhan UniversityWuhanHubei ProvinceChina Department of Rehabilitation Medicine the Fifth Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan ProvinceChina

Paired associative stimulation is a relatively new non-invasive brain stimulation technique that combines transcranial magnetic stimulation and peripheral nerve stimulation. The effects of paired associative stimulation on the excitability of the cerebral cortex can vary according to the time interval between the transcranial magnetic stimulation and peripheral nerve stimulation. We established a model of cerebral ischemia in rats via transient middle cerebral artery occlusion. We administered paired associative stimulation with a frequency of 0.05 Hz 90 times over 4 weeks. We then evaluated spatial learning and memory using the Morris water maze. Changes in the cerebral ultra-structure and synaptic plasticity were assessed via transmission electron microscopy and a 64-channel multi-electrode array. We measured mRNA and protein expression levels of brain-derived neurotrophic factor and N-methyl-D-aspartate receptor 1 in the hippocampus using a real-time polymerase chain reaction and western blot assay. Paired associative stimulation treatment significantly improved learning and memory in rats subjected to cerebral ischemia. The ultra-structures of synapses in the CA1 area of the hippocampus in rats subjected to cerebral ischemia were restored by paired associative stimulation. Long-term potentiation at synapses in the CA3 and CA1 regions of the hippocampus was enhanced as well. The protein and mRNA expression of brain-derived neurotrophic factor and N-methyl-D-aspartate receptor 1 increased after paired associative stimulation treatment. These data indicate that paired associative stimulation can protect cog-nition after cerebral ischemia. The observed effect may be mediated by increases in the mRNA and protein expression of brain-derived neurotrophic factor and N-methyl-D-aspartate receptor 1, and by enhanced synaptic plasticity in the CA1 area of the hippocampus. The animal experiments were approved by the Animal Ethics Committee of Tongji Medical College, Huazhong University of Science & Technology, China(appr

关键词： cerebral ischemia paired associative stimulation cognitive function long-term potentiation synaptic plasticity Morris water maze synaptic structure N-methyl-D-aspartic acid receptor brain-derived neurotrophic factor multi-electrode array neural regeneration

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Sodium valproate suppresses abnormal neurogenesis induced by convulsive status epilepticus

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Neural Regeneration Research 2019年第3期14卷 480-484页

作者： Peng Wu Yue Hu Xiu-Juan Li Min Cheng Li Jiang Department of Neurology Children's Hospital of Chongqing Medical University Chongqing International Science and Technology Cooperation Center for Child Development and Disorders Ministry of Education Key Laboratory of Child Development and Disorders Key Laboratory of Pediatrics in Chongqing

Status epilepticus has been shown to activate the proliferation of neural stem cells in the hippocampus of the brain, while also causing a large amount of neuronal death, especially in the subgranular zone of the dentate gyrus and the subventricular zone. Simultaneously, proliferating stem cells tend to migrate to areas with obvious damage. Our previous studies have clearly confirmed the effect of sodium valproate on cognitive function in rats with convulsive status epilepticus. However, whether neurogenesis can play a role in the antiepileptic effect of sodium valproate remains unknown. A model of convulsive status epilepticus was established in Wistar rats by intraperitoneal injection of 3 mEq/kg lithium chloride, and intraperitoneal injection of pilocarpine 40 mg/kg after 18–20 hours. Sodium valproate(100, 200, 300, 400, 500, or 600 mg/kg) was intragastrically administered six times every day(4-hour intervals) for 5 days. To determine the best dosage, sodium valproate concentration was measured from the plasma. The effective concentration of sodium valproate in the plasma of the rats that received the 300-mg/kg intervention was 82.26 ± 11.23 μg/mL. Thus, 300 mg/kg was subsequently used as the intervention concentration of sodium valproate. The following changes were seen: Recording excitatory postsynaptic potentials in the CA1 region revealed high-frequency stimulation-induced long-term potentiation. Immunohistochemical staining for BrdU-positive cells in the brain revealed that sodium valproate intervention markedly increased the success rate and the duration of induced long-term potentiation in rats with convulsive status epilepticus. The intervention also reduced the number of newborn neurons in the subgranular area of the hippocampus and subventricular zone and inhibited the migration of newborn neurons to the dentate gyrus. These results indicate that sodium valproate can effectively inhibit the abnormal proliferation and migration of neural stem cells and newborn neurons after convulsive status epileptic

关键词： nerve regeneration status epilepticus sodium valproate long-term potentiation neural stem cells neurogenesis migration subgranular zone subventricular zone neural regeneration

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MUTUAL potentiation OF THE ANA-LGSIC EFFECT OF MORPHINE MET-ENKE-PHALIN AND DYNORPHIN AND THEIR ANTAGONISM BY NALOXONE

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针刺研究 1989年第Z1期 150-151页

作者： Wang Junfeng Ren Minfeng Han Jisheng Department of Physiology Beijing Nedical University Institute of Acupuncture Science, An Hui college of Traditional Chinese Medical Institute of Basic Medical Sciences, Chinese Academy of Medical Science

The present study deals primarily with the antagonistic effect of Naloxone(NX) against mutual potentiation of morphine (Mor), mek-enkephalin (MEK)and dyno phin (Dyn) in their analgesic effects. (1) The rats were divided into 4 groups, ie. NS, NX 0. 02, 0. 1 and 0. 5mg/kggroups. A mixture of Dyn 2. 5noml and Mot 7. 5noml was injected in thebeginning via intrathecal cannulae into each rat. Percentage incrcase in TFLin all 4 groups was between 94±19% and 109±20% 10rain later. After thateach grcup was injected subcutaneously NS, NX 0.02, 0.1 and 0.5mg/kg respe-ctively and was observed continuously for 50min. The results suggest that the

关键词： morphine analgesic injected potentiation mutual opioid primarily deals continuously doses

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Transthyretin—A Key Gene Involved in Regulating Learning and Memory in Brain, and Providing Neuroprotection in Alzheimer Disease via Neuronal Synthesis of Transthyretin Protein

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Journal of Behavioral and Brain Science 2018年第2期8卷 77-92页

作者： Javed Iqbal College of Life Science Shaanxi Normal University Xi’an China

Transthyretin (TTR), a carrier protein present in the liver and choroid plexus of the brain, has been shown to be responsible for binding thyroid hormone thyroxin (T4) and retinol in plasma and cerebrospinal fluid (CSF). TTR aids in sequestering of beta-amyloid peptides Aβ deposition, and protects the brain from trauma, ischemic stroke and Alzheimer disease (AD). Accordingly, hippocampal gene expression of TTR plays a significant role in learning and memory as well as in simulation of spatial memory tasks. TTR via interacting with transcription factor CREB regulates this process and decreased expression leads to memory deficits. By different signaling pathways, like MAPK, AKT, and ERK via Src, TTR provides tropical support through megalin receptor by promoting neurite outgrowth and protecting the neurons from traumatic brain injury. TTR is also responsible for the transient rise in intracellular Ca2+ via NMDA receptor, playing a dominant role under excitotoxic conditions. In this review, we tried to shed light on how TTR is involved in maintaining normal cognitive processes, its role in learning and memory, under memory deficit conditions;by which mechanisms it promotes neurite outgrowth;and how it protects the brain from Alzheimer disease (AD).

关键词： Learning and Memory TTR—Transthyretin AD—Alzheimer Disease CSF—Cerebrospinal Fluid MAPK—Mitogen-Activated Protein Kinases CREB—cAMP Response Element Binding Protein ERK—Extracellular Receptor Kinases Aβ—Amyloid Beta LTP—Long-Term potentiation LTD—Long-Term Depression

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Simultaneous Measurement of Neural Activities of Acute Mouse Hippocampal Slices Using Multi-Electrode Array System and Laser Confocal Calcium Imaging

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Journal of Behavioral and Brain Science 2017年第2期7卷 68-78页

作者： Yuuta Hamasaki Natsumi Haba Naoki Iwata Yoshiki Uno Minoru Saito Department of Biosciences College of Humanities and Sciences Nihon University Tokyo Japan Department of Correlative Study in Physics and Chemistry Graduate School of Integrated Basic Sciences Nihon University Tokyo Japan

Recently, non-invasive, real-time and multi-point measurement of neural activities has become possible by using a multi-electrode array (MEA). Another method for multi-point measurement is the fluorescent imaging technique using voltage indicator dyes or calcium indicator dyes. Especially, calcium imaging using fluorescent calcium indicator dyes is often more useful, because they exhibit larger changes in the fluorescence intensity than voltage indicator dyes and their fluorescence changes can be detect easily. Additionally, calcium signals play key roles in the brain function, such as the long-term potentiation (LTP) in the hippocampus, and calcium imaging can be a powerful tool to elucidate the brain function. In this study, we constructed a measurement apparatus combining the MEA system and laser confocal calcium imaging and simultaneously measured electric signals and calcium signals in acute mouse hippocampal slices. The obtained results showed the availability of the present method.

关键词： Multi-Electrode Array Laser Confocal Calcium Imaging Hippocampus Acute Slice Long-Term potentiation

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