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中国神经科学学会第十二届全国学术会议

作者： Gal Richter-Levin sagol department of neurobiology and the institute for the study of affective neuroscience University of Haifa

The amygdala modulates memory processes in other brain areas and modulates emotional memory formation（i.e. "Emotional Tagging"）. Under extreme conditions amygdala modulation may lead to the formation of abnormal plasticity and to the formation of trauma-related psychopathologies. In the past we could demonstrate that priming the amygdala prior to attempts to induce long-term potentiation（LTP） in areas such as the hippocampus and m PFC, indeed modulated the level of LTP. Importantly, it was demonstrated that similar to exposure to different stressors, priming the amygdala did not simply enhance or suppress LTP, but rather had region-specific effects. For example, priming the amygdala suppressed LTP in CA1 but enhanced LTP in the dentate gyrus（DG）. These results were in full agreement with the notion that stress and trauma do not impair or enhance memory but rather modulate the way the experience is remembered. However, the amygdala is a dynamic brain region which by itself is affected by emotional experiences and being amenable to long-term plasticity. Typically in stressrelated research animals are exposure to stress and the impact of that exposure is then examined. Similarly, amygdala priming effects on plasticity in other brain areas was mainly studied by priming the amygdala once and examining the impact on LTP induction in other brain areas. These approaches fail to take into consideration the dynamic nature of responses to stress and the fact that the amygdala is amenable to plasticity which may modify the emotional response of the individual later on. In recent years, we have started to examine the possible implications of the dynamic nature of the amygdala. We have employed a range of methodologies aiming to understand the consequences of meta-plastic alterations within the amygdala on its role in emotional learning and in stress-related psychopathologies. Various methods were employed, including the use of a range of BLA-priming stimuli, exposure of animals

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Formaldehyde increases intracellular calcium concentration in primary cultured hippocampal neurons partly through NMDA receptors and T-type calcium channels

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neuroscience Bulletin 2012年第6期28卷 715-722页

作者： Ye-Nan Chi Xu Zhang Jie Cai Feng-Yu Liu Guo-Gang Xing You Wan neuroscience Research institute and department of neurobiology Peking University Key Laboratory for neuroscience Ministry of Education /Ministry of HealthPeking University

Objective Formaldehyde at high concentrations is a contributor to air pollution. It is also an endogenous metabolic product in cells, and when beyond physiological concentrations, has pathological effects on neurons. Formaldehyde induces mis-folding and aggregation of neuronal tau protein, hippocampal neuronal apoptosis, cognitive impairment and loss of memory functions, as well as excitation of peripheral nociceptive neurons in cancer pain models. Intracellular calcium （[Ca2＋]i） is an important intracellular messenger, and plays a key role in many pathological processes. The present study aimed to investigate the effect of formaldehyde on [Ca2＋]i and the possible involvement of N-methyl-D-aspartate receptors （NMDARs） and T-type Ca2＋ channels on the cell membrane. Methods Using primary cultured hippocampal neurons as a model, changes of [Ca2＋]i in the presence of formaldehyde at a low concentration were detected by confocal laser scanning microscopy. Results Formaldehyde at 1 mmol/L approximately doubled [Ca2＋]i. （2R）-amino-5-phosphonopentanoate （AP5, 25 μmol/L, an NMDAR antagonist） and mibefradil （MIB, 1 μmol/L, a T-type Ca2＋ channel blocker）, given 5 min after formaldehyde perfusion, each partly inhibited the formaldehyde-induced increase of [Ca：＋]i, and this inhibitory effect was reinforced by combined application of AP5 and MIB. When applied 3 min before formaldehyde perfusion, AP5 （even at 50μmol/L） did not inhibit the formaldehyde-induced increase of [Ca2＋]i, but MIB （1 μmol/L） significantly inhibited this increase by 70%. Conclusion These results suggest that formaldehyde at a low concentration increases [Ca2＋]i in cultured hippocampal neurons; NMDARs and T-type Ca2＋ channels may be involved in this process.

关键词： formaldehyde intracellular calcium neuronal activation NMDA receptors T-type calcium channels

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A Critical Time-Window for the Selective Induction of Hippocampal Memory Consolidation by a Brief Episode of Slow-Wave Sleep

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neuroscience Bulletin 2018年第6期34卷 1091-1099页

作者： Yi Lu Zheng-Gang Zhu Qing-Qing Ma Yun-Ting Su Yong Han Xiaodong Wang Shumin Duan Yan-Qin Yu department of neurobiology Institute of NeuroscienceNational Health Commission and Chinese Academy of Medical Sciences Key Laboratory of Medical NeurobiologyZhejiang University School of Medicine

Although extensively studied, the exact role of sleep in learning and memory is still not very clear. Sleep deprivation has been most frequently used to explore the effects of sleep on learning and memory, but the results from such studies are inevitably complicated by concurrent stress and distress. Furthermore, it is not clear whether there is a strict time-window between sleep and memory consolidation. In the present study we were able to induce time-locked slow-wave sleep(SWS) in mice by optogenetically stimulating GABAergic neurons in the parafacial zone(PZ), providing a direct approach to analyze the influences of SWS on learning and memory with precise time-windows. We found that SWS induced by light for 30 min immediately or 15 min after the training phase of the object-in-place task significantly prolonged the memory from 30 min to 6 h. However, induction of SWS 30 min after the training phase did not improve memory, suggesting a critical time-window between the induction of a brief episode of SWS and learning for memory *** of a gentle touch to the mice during light stimulation to prevent SWS induction also failed to improve memory, indicating the specific role of SWS,but not the activation of PZ GABAergic neurons itself, in memory consolidation. Similar influences of light-induced SWS on memory consolidation also occurred for Y-maze spatial memory and contextual fear memory, but not for cued fear memory. SWS induction immediately before the test phase had no effect on memory performance, indicating that SWS does not affect memory retrieval. Thus, by induction of a brief-episode SWS we have revealed a critical time window for the consolidation of hippocampusdependent memory.

关键词： Parafacial zone Slow-wave sleep Memory consolidation Hippocampus Optogenetics

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Biophotons Contribute to Retinal Dark Noise

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neuroscience Bulletin 2016年第3期32卷 246-252页

作者： Zehua Li Jiapei Dai Wuhan institute for neuroscience and Neuroengineering South Central University for Nationalities department of neurobiology College of Life SciencesSouth Central University for Nationalities

The discovery of dark noise in retinal photoreceptors resulted in a long-lasting controversy over its origin and the underlying ***,we used a novel ultra-weak biophoton imaging system（UBIS） to detect biophotonic activity（emission） under dark conditions in rat and bullfrog（Rana catesbeiana） retinas in *** found a significant temperature-dependent increase in biophotonic activity that was completely blocked either by removing intracellular and extracellular Ca^（2＋）together or inhibiting phosphodiesterase *** findings suggest that the photon-like component of discrete dark noise may not be caused by a direct contribution of the thermal activation of rhodopsin,but rather by an indirect thermal induction of biophotonic activity,which then activates the retinal chromophore of ***,this study suggests a possible solution regarding the thermal activation energy barrier for discrete dark noise,which has been debated for almost half a century.

关键词： Biophoton Rat and bullfrog retinas Retinal dark noise Phosphodiesterase 6 Ca2+ Biophoton imaging

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Disruption of dopamine D1 receptor phosphorylation at serine 421 attenuates cocaine-induced behaviors in mice

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neuroscience Bulletin 2014年第6期30卷 1025-1035页

作者： Ying Zhang Ning Wang Ping Su Jie Lu Yun Wang neuroscience Research institute and department of neurobiology The Key Laboratory for Neuroscience of the Ministry of Education/National Health and Family Planning CommissionPeking University Health Science Center PKU-IDG/Mc Govern institute for Brain Research Peking University

Dopamine D1 receptors（D1Rs） play a key role in cocaine addiction, and multiple protein kinases such as GRKs, PKA, and PKC are involved in their phosphorylation. Recently, we reported that protein kinase D1 phosphorylates the D1 R at S421 and promotes its membrane localization. Moreover, this phosphorylation of S421 is required for cocaineinduced behaviors in rats. In the present study, we generated transgenic mice over-expressing S421A-D1 R in the forebrain. These transgenic mice showed reduced phospho-D1R（S421） and its membrane localization, and reduced downstream ERK1/2 activation in the striatum. Importantly, acute and chronic cocaine-induced locomotor hyperactivity and conditioned place preference were significantly attenuated in these mice. These findings provide in vivo evidence for the critical role of S421 phosphorylation of the D1 R in its membrane localization and in cocaine-induced behaviors. Thus, S421 on the D1 R represents a potential pharmacotherapeutic target for cocaine addiction and other drug-abuse disorders.

关键词： protein kinase D1 dopamine D1 receptor phosphorylation cocaine addiction conditioned place preference locomotor activity

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Relationships among magnetic resonance imaging, histological findings, and IGF-I in steroid-induced osteonecrosis of the femoral head in rabbits

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2008年第9期9卷 739-746页

作者： Xing-can CHEN1,2, Jian WENG1, Xue-qun CHEN1, Ji-zeng DU1, Miao-ping ZHU2, Yong-qing PAN2, Miao LIU2 (1Division of neurobiology and Physiology, institute of neuroscience, School of Medicine, Zhejiang University, Hangzhou 310058, China) (2department of Radiology, the 117 Hospital of the Chinese People’s Liberation Army, Hangzhou 310013, China) Division of neurobiology and Physiology Institute of Neuroscience School of Medicine Zhejiang University Hangzhou 310058 China. genius1174@***

Objective: To study the relationships among magnetic resonance imaging (MRI), histological findings, and insu- lin-like growth factor-I (IGF-I) in steroid-induced osteonecrosis of the femoral head in rabbits. Methods: Thirty rabbits were randomly divided into experimental Group A (n=15) and control Group B (n=15). The 7.5 mg/kg (2 ml) of dexamethasone (DEX) and physiological saline (2 ml) were injected into the right gluteus medius muscle twice at one-week intervals in animals of Groups A and B, respectively. At 4, 8 and 16 weeks after obtaining an MRI, the rabbits were sacrificed and the femoral head from one side was removed for histological study of lacunae empty of osteocytes, subchondral vessels, and size of fat cells under microscopy, and the femoral head from the other side was removed for enzyme-linked immunoadsorbent assay (ELISA) for IGF-I. Results: At 4, 8 and 16 weeks after treatment, no necrotic lesions were detected in Group B, while they were detected in Group A. Light microscopy revealed that the fat cells of the marrow cavity were enlarged, subchondral vessels were evidently decreased, and empty bone lacunae were clearly increased. The IGF-I levels in Group A were significantly higher than those in Group B. At 8 weeks after the DEX injection, the MRI of all 20 femora showed an inhomogeneous, low signal intensity area in the femoral head, and at 16 weeks, the findings of all 10 femora showed a specific "line-like sign". The MRI findings of all femora in Group B were normal. Conclusion: MRI is a highly sensitive means of diagnosing early experimental osteonecrosis of the femoral head. However, the abnormal marrow tissues appeared later than 4 weeks when the expression of IGF-I increased. This reparative factor has an early and important role in response to steroid-induced osteonecrosis of the femoral head, and provides a theoretical foundation for understanding the pathology and designing new therapies.

关键词： Dexamethasone (DEX) Insulin-like growth factor-I (IGF-I) Magnetic resonance imaging (MRI) Osteonecrosis of the femoral head Pathology

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Adult Stress Promotes Purinergic Signaling to Induce Visceral Pain in Rats with Neonatal Maternal Deprivation

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neuroscience Bulletin 2020年第11期36卷 1271-1280页

作者： Shufen Hu Qian Sun Wan-Jie Du Jian Song Xin Li Ping-An Zhang Ji-Tian Xu Guang-Yin Xu Center for Translational Pain Medicine Institute of NeuroscienceSoochow UniversitySuzhou 215123China department of Physiology and neurobiology Medical College of Soochow UniversitySuzhou 215123China department of Physiology and neurobiology College of Basic Medical SciencesZhengzhou UniversityZhengzhou 450001China

Chronic visceral pain is one of the primary symptoms of patients with irritable bowel syndrome(IBS),which affects up to 15%of the population *** detailed mechanisms of visceral pain remain largely *** previous studies have shown that neonatal maternal deprivation(NMD)followed by adult multiple stress(AMS)advances the occurrence of visceral pain,likely due to enhanced norepinephrine(NE)-β2 adrenergic *** study was designed to explore the roles of P2X3 receptors(P2X3Rs)in the chronic visceral pain induced by combined ***,we showed that P2X3 Rs were co-expressed inβ2 adrenergic receptor(β2-AR)-positive dorsal root ganglion neurons and that NE significantly enhanced ATP-induced Ca2+*** and AMS not only significantly increased the protein expression of P2X3Rs,but also greatly enhanced the ATP-evoked current density,number of action potentials,and intracellular Ca2+concentration of colon-related DRG *** injection of the P2X3R inhibitor A317491 greatly attenuated the visceral pain and the ATP-induced Ca2+signals in NMD and AMS ***,theβ2-AR antagonist butoxamine significantly reversed the expression of P2X3Rs,the ATP-induced current density,and the number of action potentials of DRG ***,our data demonstrate that NMD followed by AMS leads to P2X3R activation,which is most likely mediated by upregulation ofβ2 adrenergic signaling in primary sensory neurons,thus contributing to visceral hypersensitivity.

关键词： Irritable bowel syndrome Visceral hypersensitivity β2 adrenergic receptor P2X3 receptor Dorsal root ganglion Stress

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Postnatal feeding with high-fat diet induces obesity and precocious puberty in C57BL/6J mouse pups： a novel model of obesity and puberty

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Frontiers of Medicine 2017年第2期11卷 266-276页

作者： Rahim Ullah Yan Su Yi Shen Chunlu Li Xiaoqin Xu Jianwei Zhang Ke Huang Naveed Rauf Yang He Jingjing Cheng Huaping Qin Yu-Dong Zhou Junfen Fu department of Endocrinology Children's Hospital Zhejiang University School of Medicine Hangzhou 310051 China department of neurobiology Institute of Neuroscience and the Collaborative Innovation Center for Brain Science Key Laboratory of Medical Neurobiology of the Ministry of Health of China Zhejiang University School of Medicine Hangzhou 310058 China

Childhood obesity and obesity-related metabolic complications are induced by a high-fat postnatal diet. The lack of a suitable animal model, however, remains a considerable challenge in obesity studies. In the current study, we provided high-fat diet （HFD） to dams during lactation and to pups after weaning. We also developed a novel model of C57BL/6J mouse pups with HFD-induced postnatal obesity. Results showed that feeding with HFD induces fat deposition and obesity in pups. Furthermore, HFD more potently increased the body weight （BW） of male than female pups. HFD-fed female pups were obese, underwent precocious puberty, and showed increased kisspeptin expression in the hypothalamus. However, parental obesity and precocious puberty exerted no synergistic effects on the HFD-induced postnatal weight gain and puberty onset of the pups. Interestingly, some HFD-fed litters with normal BW also exhibited precocious puberty. This finding suggested that diet composition but not BW triggers puberty onset. Our model suggests good construction validity of obesity and precocious puberty. Furthermore, our model can also be used to explore the mutual interactions between diet-induced postnatal childhood obesity and puberty.

关键词： postnatal HFD feeding obesity kisspeptin HPG axis precocious puberty

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Distributions of Visual Receptive Fields from Retinotopic to Craniotopic Coordinates in the Lateral Intraparietal Area and Frontal Eye Fields of the Macaque

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neuroscience Bulletin 2024年第2期40卷 171-181页

作者： Lin Yang Min Jin Cong Zhang Ning Qian Mingsha Zhang Key Laboratory of Cognitive neuroscience and Learning Division of PsychologyBeijing Normal UniversityBeijing 100875China institute of neuroscience Key Laboratory of Primate NeurobiologyCAS Center for Excellence in Brain Science and Intelligence TechnologyChinese Academy of SciencesShanghai 200031China department of neuroscience and Zuckerman institute Columbia UniversityNew York 10027USA

Even though retinal images of objects change their locations following each eye movement,we perceive a stable and continuous *** possible mechanism by which the brain achieves such visual stability is to construct a craniotopic coordinate by integrating retinal and extraretinal *** have been several proposals on how this may be done,including eye-position modulation(gain fields)of retinotopic receptive fields(RFs)and craniotopic *** the present study,we investigated coordinate systems used by RFs in the lateral intraparietal(LIP)cortex and frontal eye fields(FEF)and compared the two *** mapped the two-dimensional RFs of neurons in detail under two eye fixations and analyzed how the RF of a given neuron changes with eye position to determine its coordinate *** same recording and analysis procedures were applied to the two brain *** found that,in both areas,RFs were distributed from retinotopic to craniotopic *** was no significant difference between the distributions in the LIP and *** a small fraction of neurons was fully craniotopic,whereas most neurons were between the retinotopic and craniotopic *** distributions were strongly biased toward the retinotopic side but with significant craniotopic *** results suggest that there is only weak evidence for craniotopic RFs in the LIP and FEF,and that transformation from retinotopic to craniotopic coordinates in these areas must rely on other factors such as gain fields.

关键词： Reference frames Eye-centered Headcentered Visual stability

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Functional Investigation of a GRIN2A Variant Associated with Rolandic Epilepsy

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neuroscience Bulletin 2018年第2期34卷 237-246页

作者： Xing-Xing Xu Xiao-Rong Liu Cui-Ying Fan Jin-Xing Lai Yi-Wu Shi Wei Yang Tao Su Jun-Yu Xu Jian-Hong Luo Wei-Ping Liao department of neurobiology Key Laboratory of Medical Neurobiology (Ministry of Health of China) Collaborative Innovation Center for Brain Science Zhejiang University School of Medicine institute of neuroscience Department of the Second Affiliated Hospital of Guangzhou Medical University Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China

N-methyl-D-aspartate receptors（NMDARs）, a subtype of glutamate-gated ion channels, play a central role in epileptogenesis. Recent studies have identified an increasing number of GRIN2 A（a gene encoding the NMDAR GluN2A subunit） mutations in patients with epilepsy. Phenotypes of GRIN2 A mutations include epilepsy-aphasia disorders and other epileptic encephalopathies, which pose challenges in clinical treatment. Here we identified a heterozygous GRIN2 A mutation（c.1341 T[A, p.N447 K） from a boy with Rolandic epilepsy by whole-exome sequencing. The patient became seizurefree with a combination of valproate and *** investigation was carried out using recombinant NMDARs containing a GluN2A-N447 K mutant that is located in the ligand-binding domain of the GluN2A subunit. Whole-cell current recordings in HEK 293 T cells revealed that the N447 K mutation increased the NMDAR current density by;.2-fold, enhanced the glutamate potency by 2-fold, and reduced the sensitivity to Mg;inhibition. These results indicated that N447 K is a gain-offunction mutation. Interestingly, alternative substitutions by alanine and glutamic acid at the same residue（N447 A and N447 E） did not change NMDAR function, suggesting a residual dependence of this mutation in altering NMDAR function. Taken together, this study identified human GluN2A N447 K as a novel mutation associated with epilepsy and validated its functional consequences in *** of this mutation is also helpful for advancing our understanding of the role of NMDARs in epilepsy and provides new insights for precision therapeutics in epilepsy.

关键词： Epilepsy NMDA receptors GRIN2A Mutation

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