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Vascular developmental biology: getting nervous

CURRENT OPINION IN GENETICS & DEVELOPMENT 2000年第5期10卷 536-542页

作者： Shima, DT Mailhos, C Imperial Canc Res Fund Endothelial Cell Biol Lab London WC2A 3PX England Imperial Canc Res Fund Dev Genet Lab London WC2A 3PX England

First described in the developing nervous system, Semaphorin III/Neuropilin, Ephrin/Eph, and Delta/Notch signaling relays have now been implicated in the elaboration of the blood vessel network during embryogenesis.

关键词：糖蛋白类/生理学膜蛋白质类/生理学新生血管化生理性/生理学神经组织蛋白质类/生理学神经系统/胚胎学神经纤毛蛋白质1 受体 Notch 信号素3A 信号传导动物人类

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Synaptic assembly of the brain in the absence of neurotransmitter secretion

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SCIENCE 2000年第5454期287卷 864-869页

作者： Verhage, M Maia, AS Plomp, JJ Brussaard, AB Heeroma, JH Vermeer, H Toonen, RF Hammer, RE van den Berg, TK Missler, M Geuze, HJ Südhof, TC Univ Utrecht Med Ctr Rudolf Magnus Inst Utrecht Netherlands 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 Leiden Univ Med Ctr Dept Neurol Leiden Netherlands Leiden Univ Med Ctr Dept Physiol Leiden Netherlands Vrije Univ Amsterdam Inst Neurosci Dept Neurophysiol Amsterdam Netherlands Univ Texas SW Med Ctr Dept Biochem Dallas TX 75235 USA Vrije Univ Amsterdam Dept Cell Biol & Immunol Amsterdam Netherlands Univ Utrecht Dept Cell Biol Utrecht Netherlands

Brain function requires precisely orchestrated connectivity between neurons. Establishment of these connections is believed to require signals secreted from outgrowing axons, followed by synapse formation between selected neurons. Deletion of a single protein, Munc18-1, in mice Leads to a complete Loss of neurotransmitter secretion from synaptic vesicles throughout development. However, this does not prevent normal brain assembly, including formation of Layered structures, fiber pathways, and morphologically defined synapses. After assembly is completed, neurons undergo apoptosis, leading to widespread neurodegeneration. Thus, synaptic connectivity does not depend on neurotransmitter secretion, but its maintenance does. Neurotransmitter secretion probably functions to validate already established synaptic connections.

关键词：细胞凋亡脑/细胞学脑/胚胎学脑/生理学细胞分化细胞分裂基因缺失生长锥/生理学小鼠基因敲除 Munc18蛋白质类神经变性神经组织蛋白质类/遗传学神经组织蛋白质类/生理学神经通路神经肌肉接头/胚胎学神经肌肉接头/生理学神经元/细胞学神经元/生理学神经递质药/代谢膜片钳术突触/生理学突触/超微结构突触传递突触小泡/代谢突触小泡/超微结构膜泡运输蛋白质类动物小鼠

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Wind-up of spinal cord neurones and pain sensation: much ado about something?

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PROGRESS IN NEUROBIOLOGY 2000年第2期61卷 169-203页

作者： Herrero, JF Laird, JMA Lopez-Garcia, JA Univ Alcala de Henares Dept Fisiol Madrid 28871 Spain

Wind-up is a frequency-dependent increase in the excitability of spinal cord neurones, evoked by electrical stimulation of afferent C-fibres. Although it has been studied over the past thirty years, there are still uncertainties about its physiological meaning. Glutamate (NMDA) and tachykinin NK1 receptors are required to generate wind-up and therefore a positive modulation between these two receptor types has been suggested by some authors. However, most drugs capable of reducing the excitability of spinal cord neurones, including opioids and NSAIDs, can also reduce or even abolish wind-up. Thus, other theories involving synaptic efficacy, potassium channels, calcium channels, etc, have also been proposed for the generation of this phenomenon. Whatever the mechanisms involved in its generation, wind-up has been interpreted as a system for the amplification in the spinal cord of the nociceptive message that arrives from peripheral nociceptors connected to C-fibres. This probably reflects the physiological system activated in the spinal cord after an intense or persistent barrage of afferent nociceptive impulses. On the other hand, wind-up, central sensitisation and hyperalgesia are not the same phenomena, although they may share common properties. Wind-up can be an important tool to study the processing of nociceptive information in the spinal cord, and the central effects of drugs that modulate the nociceptive system. This paper reviews the physiological and pharmacological data on wind-up of spinal cord neurones, and the perceptual correlates of wind-up in human subjects, in the context of its possible relation to the triggering of hyperalgesic stales, and also the multiple factors which contribute to the generation of wind-up. (C) 2000 Elsevier Science Ltd. All rights reserved.

关键词：传入通路/生理学镇痛药/药理学麻醉药局部/药理学消炎药非甾类/药理学痛觉过敏/病理生理学炎症离子转运/药物作用模型神经学吗啡/药理学神经纤维/药物作用神经纤维/生理学神经组织蛋白质类/药物作用神经组织蛋白质类/生理学神经痛/病理生理学神经元可塑性/药物作用神经元可塑性/生理学神经元传入/药物作用神经元传入/生理学神经肽类/生理学疼痛感受器/生理学疼痛/药物疗法疼痛/病理生理学受体亲代谢性谷氨酸盐/药物作用受体亲代谢性谷氨酸盐/生理学受体 N-甲基-D-天冬氨酸/药物作用受体 N-甲基-D-天冬氨酸/生理学受体神经激肽1/药物作用受体神经激肽1/生理学反射/生理学脊髓/细胞学脊髓/病理生理学 P物质/生理学突触传递/药物作用内脏/神经支配动物猫人类

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Synaptophysin regulates clathrin-independent endocytosis of synaptic vesicles

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第11期97卷 6120-6125页

作者： Daly, C Sugimori, M Moreira, JE Ziff, EB Llinás, R NYU Med Ctr Dept Physiol & Neurosci New York NY 10016 USA NYU Med Ctr Howard Hughes Med Inst New York NY 10016 USA NYU Med Ctr Dept Biochem New York NY 10016 USA Marine Biol Lab Woods Hole MA 02543 USA Univ Sao Paulo Ribeirao Preto Med Sch Dept Morphol BR-05508 Sao Paulo Brazil

The GTPase dynamin I is required for synaptic vesicle (SV) endocytosis, Our observation that dynamin binds to the SV protein synaptophysin in a Ca2+-dependent fashion suggested the possibility that a dynamin/synaptophysin complex functions in SV recycling, In this paper we show that disruption of the dynamin/synaptophysin interaction by peptide injection into the squid giant synapse preterminal results in a decrease in transmitter release during high-frequency stimulation, indicating an inhibition of SV recycling, Electron microscopy of these synapses reveals a depletion of SVs. demonstrating a block of vesicle retrieval after fusion, In addition, we observed an increase in clathrin-coated vesicles, indicating that the peptide does not block clathrin-dependent endocytosis, We conclude that the dynamin/synaptophysin complex functions in a clathrin-independent mechanism of SV endocytosis that is required for efficient synaptic transmission.

关键词：钙/生理学网格蛋白/生理学十腕总目动力蛋白质Ⅰ 动力蛋白质类胞吞作用/生理学 GTP磷酸水解酶类/生理学大分子物质膜融合神经组织蛋白质类/生理学重组融合蛋白质类/生理学星状神经节/细胞学突触传递/生理学突触小泡/生理学突触囊泡蛋白/生理学动物

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Proteomic analysis of NMDA receptor-adhesion protein signaling complexes

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NATURE NEUROSCIENCE 2000年第7期3卷 661-669页

作者： Husi, H Ward, MA Choudhary, JS Blackstock, WP Grant, SGN Univ Edinburgh Ctr Neurosci Ctr Genome Res Edinburgh EH9 3JQ Midlothian Scotland Glaxo Wellcome Res & Dev Ltd Stevenage SG1 2NY Herts England

N-methyl-D-aspartate receptors (NMDAR) mediate long-lasting changes in synapse strength via downstream signaling pathways. We report proteomic characterization with mass spectrometry and immunoblotting of NMDAR multiprotein complexes (NRC) isolated from mouse brain. The NRC comprised 77 proteins organized into receptor, adaptor, signaling, cytoskeletal and novel proteins, of which 30 are implicated from binding studies and another 19 participate in NMDAR signaling. NMDAR and metabotropic glutamate receptor subtypes were linked to cadherins and L1 cell-adhesion molecules in complexes lacking AMPA receptors. These neurotransmitter-adhesion receptor complexes were bound to kinases, phosphatases, GTPase-activating proteins and Ras with effecters including MAPK pathway components. Several proteins were encoded by activity-dependent genes. Genetic or pharmacological interference with 15 NRC proteins impairs learning and with 22 proteins alters synaptic plasticity in rodents. Mutations in three human genes (NF1, Rsk-2 L1) are associated with learning impairments, indicating the NRC also participates in human cognition.

关键词：脑/生理学钙黏着糖蛋白类/化学钙黏着糖蛋白类/生理学细胞支架蛋白质类/化学细胞支架蛋白质类/生理学质谱分析法神经组织蛋白质类/化学神经组织蛋白质类/遗传学神经组织蛋白质类/生理学神经递质药/化学神经递质药/生理学蛋白激酶类/化学蛋白激酶类/代谢受体 N-甲基-D-天冬氨酸/化学受体 N-甲基-D-天冬氨酸/生理学信号传导/生理学动物人类小鼠

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Loss of autoreceptor functions in mice lacking the dopamine transporter

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NATURE NEUROSCIENCE 1999年第7期2卷 649-655页

作者： Jones, SR Gainetdinov, RR Hu, XT Cooper, DC Wightman, RM White, FJ Caron, MG Duke Univ Med Ctr Dept Cell Biol Howard Hughes Med Inst Durham NC 27710 USA Finch Univ Hlth Sci Chicago Med Sch N Chicago IL 60064 USA Univ N Carolina Dept Chem Chapel Hill NC 27599 USA Univ N Carolina Curriculum Neurobiol Chapel Hill NC 27599 USA

Autoreceptors provide an important inhibitory feedback mechanism for dopamine neurons by altering neuronal functions in response to changes in extracellular levels of dopamine. Elevated dopamine may be a component of several neuropsychiatric disorders. However, evidence concerning the state of autoreceptors in such conditions has remained elusive. The function of dopamine autoreceptors was assessed in mice lacking the dopamine transporter (DAT). Genetic deletion of the DAT gene in mice results in a persistent elevation in levels of extracellular dopamine. Direct assessment of impulse-, synthesis- and release-regulating autoreceptors in these mice reveals a nearly complete loss of function. These findings may provide insight into the neurochemical consequences of hyperdopaminergia.

关键词： 3 4-二羟苯酰乙酸/代谢放射自显影术脑/生理学载体蛋白质类/遗传学载体蛋白质类/生理学多巴胺/代谢多巴胺激动剂/药代动力学多巴胺质膜转运蛋白质类电刺激反馈/生理学基因缺失高香草酸/代谢碘放射性同位素膜糖蛋白类膜转运蛋白质类中脑/代谢小鼠近交C57BL 小鼠基因敲除微透析神经组织蛋白质类/缺乏神经组织蛋白质类/生理学神经元/药物作用神经元/生理学喹吡罗/药理学受体多巴胺D2/代谢水杨酰胺类/药代动力学动物小鼠

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Dopamine transporters participate in the physiological regulation of prolactin

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ENDOCRINOLOGY 2000年第1期141卷 366-374页

作者： Demaria, JE Nagy, GM Lerant, AA Fekete, MIE Levenson, CW Freeman, ME Florida State Univ Dept Biol Sci Tallahassee FL 32306 USA Florida State Univ Dept Nutr Food & Exercise Sci Program Neurosci Tallahassee FL 32306 USA Semmelweis Univ Neuroendocrine Res Lab Dept Human Morphol & Embryol H-1085 Budapest Hungary Hungarian Acad Sci Inst Expt Med Budapest Hungary

Three populations of hypothalamic neuroendocrine dopaminergic (NEDA) neurons, arising from the arcuate and periventricular nuclei of the hypothalamus release dopamine (DA) that acts at the pituitary gland to regulate the secretion of PRL. It is generally accepted that NEDA neurons lack functional DA transporters (DATs), which are responsible for uptake of DA from the synaptic cleft into the presynaptic axon terminal. This study localized DATs to the hypothalamopituitary axis and evaluated the effect of DAT blockade on the hypothalamo-pituitary regulation of PRL. After 7 days of treatment with cocaine (a nonspecific amine transporter blocker) or mazindol(a specific DAT blocker), the relative abundance of PRL messenger RNA (mRNA) in the anterior lobe (AL) of OVX rats was significantly decreased, whereas the relative abundance of tyrosine hydroxylase mRNA in the hypothalamus was significantly increased. The effect of cocaine or mazindol administration on DA turnover and serum PRL concentration was examined in estradiol (E-2)- treated OVX rats. E-2 administration (iv) resulted in a significant increase in serum PRL within 4 h;however, cocaine or mazindol administration abolished the E-2-induced increase of PRL. Cocaine or mazindol significantly increased the concentration of DA at the site of the axon terminals within the median eminence (ME), intermediate lobe (IL) and neural lobe (NL), indicating blockade of uptake. Because formation of DOPAC requires uptake of DA, concentrations of DOPAC in the ME, IL and NL decreased following treatment with either cocaine or mazindol. These data, together with the presence of immunopositive DAT in the ME, pituitary stalk, IL, and NL, suggest that a functional DAT system is present within all three populations of NEDA neurons. Moreover, similarity between the effects of cocaine and mazindol treatment indicate that blockade of the DAT, but not other amine transporters, is responsible for suppression of PRL gene expression and secreti

关键词： 3 4-二羟苯酰乙酸/代谢脑/细胞学脑/代谢载体蛋白质类/生理学可卡因/药理学多巴胺/代谢多巴胺/生理学多巴胺质膜转运蛋白质类多巴胺摄取抑制剂/药理学雌二醇/药理学下丘脑-垂体系统/生理学免疫组织化学马吲哚/药理学正中隆起/代谢膜糖蛋白类膜转运蛋白质类神经组织蛋白质类/生理学神经分泌系统/细胞学神经分泌系统/代谢催乳素/生物合成催乳素/代谢大鼠 Sprague-Dawley 酪氨酸单氧化酶/代谢动物女(雌)性大鼠

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Slit branches out: A secreted protein mediates both attractive and repulsive axon guidance

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CELL 1999年第1期97卷 1-4页

作者： Zinn, K Sun, Q CALTECH Div Biol Pasadena CA 91125 USA

Investigates the potential relationship between the extracellular matrix protein Slit and Robo as receptor in the extracellular matrix. Binding to Robo-expressing cells in fly and vertebrate proteins; Slit's repul... 详细信息

关键词：轴突/生理学果蝇属/胚胎学果蝇蛋白质类神经组织蛋白质类/生理学神经组织蛋白质类/分泌动物人类

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G-protein-independent signaling by G-protein-coupled receptors

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TRENDS IN NEUROSCIENCES 2000年第10期23卷 469-475页

作者： Heuss, C Gerber, U Univ Zurich Brain Res Inst CH-8057 Zurich Switzerland

Two classes of receptors transduce neurotransmitter signals: ionotropic receptors and heptahelical metabotropic receptors. Whereas the ionotropic receptors are structurally associated with a membrane channel, a mediating mechanism is necessary to functionally link metabotropic receptors with their respective effecters. According to the accepted paradigm, the first step in the metabotropic transduction process requires the activation of heterotrimeric G-proteins, An increasing number of observations, however, point to a novel mechanism through which neurotransmitters can initiate biochemical signals and modulate neuronal excitability, According to this mechanism metabotropic receptors induce responses by activating transduction systems that do not involve G-proteins.

关键词：基因表达调控异源三聚体GTP结合蛋白质类/生理学无脊椎动物/生理学 MAP激酶信号系统/药物作用模型神经学神经组织蛋白质类/生理学神经递质药/药理学受体蛋白质酪氨酸激酶类/生理学受体生长因子/生理学受体亲代谢性谷氨酸盐/药物作用受体亲代谢性谷氨酸盐/生理学受体神经递质/分类受体神经递质/药物作用受体神经递质/生理学信号传导/药物作用信号传导/生理学突触传递/药物作用突触传递/生理学转录激活脊椎动物/生理学 src族激酶类/生理学动物人类

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(Over)correction of FMR1 deficiency with YAC transgenics: behavioral and physical features

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HUMAN MOLECULAR GENETICS 2000年第8期9卷 1145-1159页

作者： Peier, AM McIlwain, KL Kenneson, A Warren, ST Paylor, R Nelson, DL Baylor Coll Med Dept Mol & Human Genet Houston TX 77030 USA Emory Univ Sch Med Dept Chem Atlanta GA 30322 USA Emory Univ Sch Med Howard Hughes Med Inst Atlanta GA 30322 USA

Fragile X syndrome is a common cause of mental retardation involving loss of expression of the FMR1 gene. The role of FMR1 remains undetermined but the protein appears to be involved in RNA metabolism. Fmr1 knock-out mice exhibit a phenotype with some similarities to humans, such as macroorchidism and behavioral abnormalities. As a step toward understanding the function of FMR1 and the determination of the potential for therapeutic approaches to fragile X syndrome, yeast artificial chromosome (YAC) transgenic mice were generated in order to determine whether the Fmr1 knockout mouse phenotype could be rescued. Several transgenic lines were generated that carried the entire FMR1 locus with extensive amounts of flanking sequence. We observed that the YAC transgene supported production of the human protein (FMRP) which was present at levels 10 to 15 times that of endogenous protein and was expressed in a cell- and tissue-specific manner. Macroorchidism was absent in knockout mice carrying the YAC transgene indicating functional rescue by the human protein. Given the complex behavioral phenotype in fragile X patients and the mild phenotype previously reported for the Fmr1 knockout mouse, we performed a more thorough evaluation of the Fmr1 knockout phenotype using additional behavioral assays that had not previously been reported for this animal model. The mouse displayed reduced anxiety-related responses with increased exploratory behavior. FMR1 YAC transgenic mice overexpressing the human protein did produce opposing behavioral responses and additional abnormal behaviors were also observed. These findings have significant implications for gene therapy for fragile X syndrome since overexpression of the gene may harbor its own phenotype.

关键词：脑/代谢染色体人工酵母外显子脆性X智力低下蛋白质脆性X综合征/遗传学脆性X综合征/治疗基因疗法精神障碍/遗传学小鼠基因敲除小鼠转基因运动活动神经组织蛋白质类/缺乏神经组织蛋白质类/遗传学神经组织蛋白质类/生理学表型 RNA结合蛋白质类重组蛋白质类/生物合成睾丸/代谢动物人类男(雄)性小鼠

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