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Can molecules explain long-term potentiation?

NATURE NEUROSCIENCE 1999年第7期2卷 597-604页

作者： Sanes, JR Lichtman, JW Washington Univ Sch Med Dept Anat & Neurobiol St Louis MO 63110 USA

Although over 100 molecules have been Implicated in long-term potentiation and depression, no consensus on their underlying molecular mechanisms has emerged. Here we discuss the difficulties of providing molecular exp... 详细信息

关键词：海马/生理学长时程增强/生理学模型神经学神经组织蛋白质类/生理学神经递质药/生理学受体谷氨酸/生理学动物人类

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Dendritic spine structural anomalies in fragile-X mental retardation syndrome

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CEREBRAL CORTEX 2000年第10期10卷 1038-1044页

作者： Irwin, SA Galvez, R Greenough, WT Univ Illinois Beckman Inst Urbana IL 61801 USA Univ Illinois Dept Psychol Neurosci Program Urbana IL 61801 USA Univ Illinois Dept Psychol Med Scholars Programs Urbana IL 61801 USA Univ Illinois Dept Psychiat Urbana IL 61801 USA Univ Illinois Dept Cell & Struct Biol Urbana IL 61801 USA

Fragile-X syndrome is the most common single-gene inherited form of mental retardation. Morphological studies suggest a possible failure of the synapse maturation process. Cerebral cortical spine morphology in fragile-X syndrome and in a knockout mouse model of it appears immature, with long, thin spines much more common than the stubby and mushroom-shaped spines more characteristic of normal development. In human fragile-X syndrome there is also a higher density of spines along dendrites, suggesting a possible failure of synapse elimination. While variously misshapen spines are characteristic of a number of mental retardation syndromes, the overabundance of spines seen in fragile-X syndrome is unusual. Taken with evidence of neurotransmitter activation of the synthesis of the fragile-X protein (FMRP) at synapses in vitro and evidence for behaviorally induced FMRP expression in vivo, and with evidence compatible with a role for FMRP in regulating the synthesis of other proteins, it is possible that FMRP serves as an 'immediate early protein' at the synapse that orchestrates aspects of synaptic development and plasticity.

关键词：脑/病理学树突/超微结构脆性X智力低下蛋白质脆性X综合征/并发症智力障碍/遗传学智力障碍/病理学神经组织蛋白质类/生理学 RNA结合蛋白质类突触/生理学人类

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Small GTPase RhoG is a key regulator for neurite outgrowth in PC12 cells

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MOLECULAR AND CELLULAR BIOLOGY 2000年第19期20卷 7378-7387页

作者： Katoh, H Yasui, H Yamaguchi, Y Aoki, J Fujita, H Mori, K Negishi, M Kyoto Univ Mol Neurobiol Lab Grad Sch Biostudies Sakyo Ku Kyoto 6068502 Japan

The Rho family of small GTPases has been implicated in cytoskeletal reorganization and subsequent morphological changes in various cell types. Among them, Rac and Cdc42 have been shown to be involved in neurite outgrowth in neuronal cells. In this study, we examined the role of RhoG, another member of Rho family GTPases, in nerve growth factor (NGF)-induced neurite outgrowth in PC12 cells. Expression of wild-type RhoG in PC12 cells induced neurite outgrowth in the absence of NGF, and the morphology of wild-type RhoG-expressing cells was similar to that of NGF-differentiated cells. Constitutively active RhoG-transfected cells extended short neurites but developed large lamellipodial or filopodial structures at the tips of neurites. RhoG-induced neurite outgrowth was inhibited by coexpression with dominant-negative Rac1 or Cdc42. In addition expression of constitutively active RhoG elevated endogenous Rac1 and Cdc42 activities. We also found that the NGF-induced neurite outgrowth was enhanced by expression of wild-type RhoG whereas expression of dominant-negative RhoG suppressed the neurite outgrow th. Furthermore, constitutively active pas-induced neurite outgrowth was also suppressed by dominant-negative RhoG. Taken together, these results suggest that RhoG is a key regulator in NGF-induced neurite outgrowth, acting downstream of Ras and upstream of Rac1 and Cdc42 in PC12 cells.

关键词：细胞分化/药物作用 GTP磷酸水解酶类/生物合成 GTP磷酸水解酶类/遗传学 GTP磷酸水解酶类/生理学基因显性诱变定点肿瘤蛋白质类/生理学神经生长因子类/药理学神经组织蛋白质类/生理学神经突/代谢 PC12细胞/药物作用 PC12细胞/代谢 PC12细胞/超微结构重组融合蛋白质类/生理学信号传导转染 cdc42GTP结合蛋白质/生理学 rac1GTP结合蛋白质/生理学动物大鼠

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The synaptic glycoprotein neuroplastin is involved in long-term potentiation at hippocampal CA1 synapses

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第8期97卷 4327-4332页

作者： Smalla, KH Matthies, H Langnäse, K Shabir, S Böckers, TW Wyneken, U Staak, S Krug, M Beesley, PW Gundelfinger, ED Leibniz Inst Neurobiol D-39118 Magdeburg Germany Otto Von Guericke Univ Inst Pharmacol & Toxicol D-39120 Magdeburg Germany Otto Von Guericke Univ Inst Med Neurobiol D-39120 Magdeburg Germany Univ London Royal Holloway & Bedford New Coll Sch Biol Sci Egham TW20 0EX Surrey England Univ Munster Inst Anat D-48149 Munster Germany

Neuroplastin-65 and -55 (previously known as gp65 and gp55) are glycoproteins of the Ig superfamily that are enriched in rat forebrain synaptic membrane preparations. Whereas the two-Ig domain isoform neuroplastin-55 expressed in many tissues, the three-Ig domain isoform neuroplastin-65 is brain-specific and enriched in postsynaptic density (PSD) protein preparations. Here, we have assessed the function of neuroplastin in long-term synaptic plasticity. Immunocytochemical studies with neuroplastin-65-specific antibodies differentially stain distinct synaptic neuropil regions of the rat hippocampus with most prominent immunoreactivity in the CA1 region and the proximal molecular layer of the dentate gyrus, Kainate-induced seizures cause a significant enhancement of neuroplastin-65 association with PSDs. Similarly, long-term potentiation (LTP) of CA1 synapses in hippocampal slices enhanced the association of neuroplastin-65 with a detergent-insoluble PSD-enriched protein fraction. Several antibodies against the neuroplastins, including one specific for neuroplastin-65, inhibited the maintenance of LTP, A similar effect was observed when recombinant fusion protein containing the three extracellular Ig domains of neuroplastin-65 was applied to hippocampal slices before LTP induction. Microsphere binding experiments using neuroplastin-F-c chimeric proteins show that constructs containing Ig1-3 or Ig1 domains, but not Ig2-3 domains mediate hemophilic adhesion. These data suggest that neuroplastin plays an essential role in implementing long-term changes in synaptic activity, possibly by means of a hemophilic adhesion mechanism.

关键词：抗体/免疫学海马/生理学免疫球蛋白类/免疫学免疫球蛋白类/代谢免疫球蛋白类/生理学免疫组织化学长时程增强/生理学膜糖蛋白类/免疫学膜糖蛋白类/代谢膜糖蛋白类/生理学神经组织蛋白质类/免疫学神经组织蛋白质类/代谢神经组织蛋白质类/生理学前脑/代谢大鼠 Wistar 重组融合蛋白质类/代谢突触/生理学动物男(雄)性大鼠

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Cellular and molecular mechanisms of dendrite growth

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CEREBRAL CORTEX 2000年第10期10卷 963-973页

作者： McAllister, AK Univ Calif Davis Ctr Neurosci Davis CA 95616 USA

Proper growth and branching of dendrites are crucial for nervous system function;patterns of dendritic arborization determine the nature and amount of innervation that a neuron receives and specific dendritic membrane properties define its computational capabilities. Until recently, there was relatively little known about the cellular and molecular mechanisms of dendritic growth, perhaps because dendrites were historically considered to he intrinsically determined, passive elements in the formation of connections in the nervous system. In the last few years, however, overwhelming evidence has accumulated indicating that dendritic growth is remarkably dynamic and responsive to environmental signals, including guidance molecules and levels and patterns of activity. This manuscript reviews our current understanding of the cellular and molecular mechanisms of dendritic growth, the influence of activity in sculpting specific patterns of dendritic arbors, and a potential integral role for dendrites in activity-dependent development of circuits in the nervous system.

关键词：树突/生理学细胞外间隙/代谢细胞内液/代谢模型神经学神经组织蛋白质类/生理学信号传导/生理学突触/生理学动物人类

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Three-dimensional structure of the neuronal-Sec1-syntaxin 1a complex

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NATURE 2000年第6776期404卷 355-362页

作者： Misura, KMS Scheller, RH Weis, WI Stanford Univ Sch Med Dept Biol Struct Stanford CA 94305 USA Stanford Univ Sch Med Howard Hughes Med Inst Stanford CA 94305 USA

Syntaxin 1a and neuronal Sec1 (nSec1) form an evolutionarily conserved heterodimer that is essential for vesicle trafficking and membrane fusion. The crystal structure of the nSec1-syntaxin la complex, determined at 2.6 Angstrom resolution, reveals that major conformational rearrangements occur in syntaxin relative to both the core SNARE complex and isolated syntaxin. We identify regions of the two proteins that seem to determine the binding specificity of particular Sec1 proteins for syntaxin isoforms, which is likely to be important for the fidelity of membrane trafficking. The structure also indicates mechanisms that might couple the action of upstream effector proteins to conformational changes in syntaxin la and nSec1 that lead to core complex formation and membrane fusion.

关键词：氨基酸序列抗原表面/化学抗原表面/遗传学抗原表面/代谢抗原表面/生理学结合部位克隆分子结晶学 X线静电学大肠杆菌大分子物质膜融合/生理学膜蛋白质类/化学膜蛋白质类/代谢膜蛋白质类/生理学模型分子分子序列数据 Munc18蛋白质类神经组织蛋白质类/化学神经组织蛋白质类/遗传学神经组织蛋白质类/代谢神经组织蛋白质类/生理学点突变蛋白质结合蛋白质构象蛋白质亚型/化学蛋白质亚型/代谢重组蛋白质类/化学重组蛋白质类/代谢 SNARE蛋白质类序列比对突触融合蛋白质1 膜泡运输蛋白质类动物大鼠

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SV2A and SV2B function as redundant Ca²⁺ regulators in neurotransmitter release

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NEURON 1999年第4期24卷 1003-1016页

作者： Janz, R Goda, Y Geppert, M Missler, M Südhof, TC Univ Texas SW Med Ctr Howard Hughes Med Inst Ctr Basic Neurosci Dallas TX 75235 USA Univ Texas SW Med Ctr Dept Mol Genet Dallas TX 75235 USA Univ Calif San Diego Dept Biol La Jolla CA 92093 USA Max Planck Inst Expt Med Dept Mol Neurobiol D-37075 Gottingen Germany

SV2 proteins are abundant synaptic vesicle proteins expressed in two major (SV2A and SV2B) and one minor isoform (SV2C) that resemble transporter proteins. We now show that SV2B knockout mice are phenotypically normal while SV2A- and SV2A/SV2B double knockout mice exhibit severe seizures and die postnatally. In electrophysiological recordings from cultured hippocampal neurons, SV2A- or SV2B-deficient cells exhibited no detectable abnormalities. Neurons lacking both SV2 isoforms, however, experienced sustained increases in Ca2+-dependent synaptic transmission when two or more action potentials were triggered in succession. These increases could be reversed by EGTA-AM. Our data suggest that without SV2 proteins, presynaptic Ca2+ accumulation during consecutive action potentials causes abnormal increases in neurotransmitter release that destabilize synaptic circuits and induce epilepsy.

关键词：脑化学/遗传学脑化学/生理学钙信号/生理学螯合剂/药理学克隆分子依他酸/药理学电生理学胞吞作用/生理学胞吐作用/生理学外显子海马/细胞学海马/生理学内含子膜糖蛋白类/遗传学膜糖蛋白类/生理学小鼠基因敲除分子序列数据突变神经组织蛋白质类/遗传学神经组织蛋白质类/生理学神经递质药/遗传学神经递质药/代谢神经递质药/生理学发作/病理生理学突触/生理学体重减轻/生理学动物小鼠

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Mammalian ELAV-like neuronal RNA-binding proteins HuB and HuC promote neuronal development in both the central and the peripheral nervous systems

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 1999年第17期96卷 9885-9890页

作者： Akamatsu, W Okano, HJ Osumi, N Inoue, T Nakamura, S Sakakibara, SI Miura, M Matsuo, N Darnell, RB Okano, H Osaka Univ Grad Sch Med Biomed Res Ctr Dept Neuroanat Suita Osaka 5650871 Japan Keio Univ Sch Med Dept Pediat Shinjuku Ku Tokyo 1608582 Japan Japan Sci & Technol Corp CREST Minato Ku Tokyo 1050011 Japan Rockefeller Univ Lab Mol Neurooncol New York NY 10021 USA Natl Ctr Neurol & Psychiat Natl Inst Neurosci Div Biochem & Cell Biol Kodaira Tokyo 1878502 Japan

Hu proteins are mammalian embryonic lethal abnormal visual system (ELAV)-like neuronal RNA-binding proteins that contain three RNA recognition motifs, Although Drosophila ELAV is required for the correct differentiation and survival of neurons, the roles played by the Hu genes in the mammalian nervous system remain largely unknown, To explore the in vivo functions of mouse Hu proteins, we overexpressed them in rat pheochromocytoma PC12 cells, where they induced neuronal phenotype in the absence of nerve growth factor, We have characterized the functions of various forms of mHuB and mHuC bearing point mutations or deletions. Mutants of mHuC that had amino acid exchanges in the RNP1 domain of the first or second RNA recognition motifs (RRMs) lost biologic activity as well as RNA-binding activity. In addition, the mutants containing only the third RRM failed to induce the neuronal phenotype in PC12 cells and inhibited the biologic activity of cotransfected wild-type mHuB and mHuC, thus acting as a dominant-negative form. However, these mutants could not suppress the nerve growth factor-induced differentiation of PC12 cells. Further, we misexpressed wild-type and dominant-negative Hu in E9.5 mouse embryos, by using electroporation into the neural tube at the level of the rhombencephalon. mHuB and mHuC induced the ectopic expression of neuronal markers, whereas the dominant-negative forms of mHuB and mHuC suppressed the differentiation of central nervous system motor neurons, From these results, we suggest that Hu proteins are required for neuronal differentiation in the mammalian nervous system.

关键词：抗原表面/遗传学抗原表面/生理学中枢神经系统/生长和发育 DNA突变分析神经组织蛋白质类/遗传学神经组织蛋白质类/生理学神经元/生理学 PC12细胞周围神经系统/生长和发育表型 RNA结合蛋白质类/遗传学 RNA结合蛋白质类/生理学核糖核蛋白类/生理学动物小鼠大鼠

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Deficits in memory and motor performance in synaptotagmin IV mutant mice

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第10期97卷 5598-5603页

作者： Ferguson, GD Anagnostaras, SG Silva, AJ Herschman, HR Univ Calif Los Angeles Inst Mol Biol Los Angeles CA 90095 USA Univ Calif Los Angeles Dept Biol Chem Los Angeles CA 90095 USA Univ Calif Los Angeles Dept Neurobiol Los Angeles CA 90095 USA Univ Calif Los Angeles Dept Psychiat Los Angeles CA 90095 USA Univ Calif Los Angeles Dept Psychol Los Angeles CA 90095 USA Univ Calif Los Angeles Dept Pharmacol Los Angeles CA 90095 USA Univ Calif Los Angeles Brain Res Inst Los Angeles CA 90095 USA

Synaptotagmin (Syt) TV is a synaptic vesicle protein. Syt IV expression is induced in the rat hippocampus after systemic kainic acid treatment. To examine the functional role of this protein in vivo, we derived Syt IV null [Syt IV(-/-)] mutant mice. Studies with the rotorod revealed that the Syt IV mutants have impaired motor coordination, a result consistent with constitutive Syt IV expression in the cerebellum. Because Syt IV is thought to modulate synaptic function, we also have examined Syt IV mutant mice in learning and memory tests. Our studies show that the Syt IV mutation disrupts contextual fear conditioning, a learning task sensitive to hippocampal and amygdala lesions. In contrast, cued fear conditioning is normal in the Syt IV mutants, suggesting that this mutation did not disrupt amygdala function. Conditioned taste aversion, which also depends on the amygdala, is normal in the Syt IV mutants. Consistent with the idea that the Syt IV mutation preferentially affects hippocampal function, Syt IV mutant mice also display impaired social transmission of food preference. These studies demonstrate that Syt IV is critical for brain function and suggest that the Syt IV mutation affects hippocampal-dependent reaming and memory, as well as motor coordination.

关键词：声刺激钙结合蛋白质类条件反射经典/生理学提示恐惧/生理学偏食纯合子行走膜糖蛋白类/缺乏膜糖蛋白类/遗传学膜糖蛋白类/生理学记忆/生理学记忆障碍/遗传学小鼠基因敲除运动活动/遗传学运动活动/生理学神经组织蛋白质类/缺乏神经组织蛋白质类/遗传学神经组织蛋白质类/生理学反射社会行为突触结合蛋白质类味觉动物小鼠大鼠

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Live or let die -: retinal ganglion cell death and survival during development and in the lesioned adult CNS

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TRENDS IN NEUROSCIENCES 2000年第10期23卷 483-490页

作者： Bähr, M Univ Tubingen Neurol Klin D-72076 Tubingen Germany

Programmed cell death or apoptosis is a common and widespread phenomenon that is important for proper development of the nervous system. In the adult CNS, however, apoptosis contributes to secondary cell loss after various types of lesions. The retino-tectal system has been successfully used as a convenient model system to study the molecular mechanisms of neuronal apoptosis and survival during development and in the lesioned adult CNS. This review describes the current knowledge about the interactions of cell death and survival pathways in general and for retinal ganglion cells specifically.

关键词：细胞凋亡/生理学凋亡蛋白酶活化因子1 脑损伤/病理学脑源性神经营养因子/药理学脑源性神经营养因子/生理学秀丽新小杆线虫/细胞学秀丽新小杆线虫/胚胎学秀丽新小杆线虫/生长和发育载体蛋白质类/遗传学载体蛋白质类/生理学半胱氨酸天冬氨酸蛋白酶/缺乏半胱氨酸天冬氨酸蛋白酶/遗传学半胱氨酸天冬氨酸蛋白酶/生理学细胞存活基因 bcl-2 蠕虫蛋白质类/生理学小鼠基因敲除线粒体/生理学形态发生神经组织蛋白质类/缺乏神经组织蛋白质类/遗传学神经组织蛋白质类/生理学蛋白质类/遗传学蛋白质类/生理学原癌基因蛋白质类/缺乏原癌基因蛋白质类/遗传学原癌基因蛋白质类/生理学原癌基因蛋白质c-bcl-2/缺乏原癌基因蛋白质c-bcl-2/遗传学原癌基因蛋白质c-bcl-2/生理学视网膜/细胞学视网膜/胚胎学视网膜/生长和发育视网膜神经节细胞/细胞学视网膜神经节细胞/代谢视网膜神经节细胞/病理学 bcl-2相关X蛋白质 bcl相关死亡蛋白质 bcl-X蛋白质成年人动物鸡胚人类小鼠

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