Perspectives on developmental neurobiology最新文献_第6页

Signal transduction in vertebrate growth cones navigating in vivo. 脊椎动物生长锥在体内导航的信号转导。

Perspectives on developmental neurobiology Pub Date : 1996-01-01

C B Chien, W A Harris

{"title":"Signal transduction in vertebrate growth cones navigating in vivo.","authors":"C B Chien, W A Harris","doi":"","DOIUrl":"","url":null,"abstract":"Navigating growth cones need signal transduction machinery to amplify and transmit the effects of extracellular signals throughout the growth cone. In culture, many drugs that affect second messengers are known to modulate neurite extension (with different effects on different neurons), and gradients of calcium influx and cyclic nucleotide analogs can cause growth cones to turn. However, it is not clear which of these responses are physiologically relevant, as axons grow through much more complex environments in vivo. The \"exposed brain\" preparation in Xenopus embryos provides an experimentally tractable system in which it is possible to study growth, pathfinding, and target recognition of retinal growth cones in vivo, while pharmacologically manipulating their signal transduction systems. These growth cones can also be easily studied in explant culture. We describe preliminary results of parallel in vivo and in vitro experiments using an array of drugs that perturb transduction molecules. Surprisingly, calcium ionophores and cyclic nucleotide analogs have no significant effect on retinal axon growth or pathfinding. Several agents including herbimycin A, ML-7, mastoparan, and RHC80267 inhibit retinal axon growth, both in vivo and in vitro, suggesting that tyrosine kinases, myosin, heterotrimeric G-proteins, and diacylglycerol lipase are important for retinal growth cones navigating in the optic pathway.","PeriodicalId":77321,"journal":{"name":"Perspectives on developmental neurobiology","volume":"4 2-3","pages":"253-66"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20115141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The cytoskeleton in nerve growth cone motility and axonal pathfinding. 神经生长中的细胞骨架、锥体运动和轴突寻路。

Perspectives on developmental neurobiology Pub Date : 1996-01-01

P C Letourneau

引用次数: 0

Microtubule-associated proteins, phosphorylation gradients, and the establishment of neuronal polarity. 微管相关蛋白，磷酸化梯度，和神经元极性的建立。

Perspectives on developmental neurobiology Pub Date : 1996-01-01

J W Mandell, G A Banker

引用次数: 0

Tyrosine phosphorylation and protrusive structures of the growth cone. 酪氨酸磷酸化和生长锥的突出结构。

Perspectives on developmental neurobiology Pub Date : 1996-01-01

D J Goldberg, D Y Wu

引用次数: 0

Changes in neuropeptide phenotype after axotomy of adult peripheral neurons and the role of leukemia inhibitory factor. 成人外周神经元轴切术后神经肽表型的变化及白血病抑制因子的作用。

Perspectives on developmental neurobiology Pub Date : 1996-01-01

R E Zigmond, H Hyatt-Sachs, R P Mohney, R C Schreiber, A M Shadiack, Y Sun, S A Vaccariello

引用次数: 0

Calcium and chemotropic turning of nerve growth cones. 神经生长锥的钙和趋化转向

Perspectives on developmental neurobiology Pub Date : 1996-01-01

J Q Zheng, M M Poo, J A Connor

引用次数: 0

The chronotopic reordering of optic axons. 视轴突的时位重排序。

Perspectives on developmental neurobiology Pub Date : 1996-01-01

B E Reese

引用次数: 0

On the track of cell survival pharmaceuticals in the oligodendrocyte type-2 astrocyte lineage. 少突胶质细胞2型星形胶质细胞系细胞存活药物的研究进展。

Perspectives on developmental neurobiology Pub Date : 1996-01-01

M Noble, M Mayer-Próschel

{"title":"On the track of cell survival pharmaceuticals in the oligodendrocyte type-2 astrocyte lineage.","authors":"M Noble, M Mayer-Próschel","doi":"","DOIUrl":"","url":null,"abstract":"The identification of compounds that can protect cells against death induced by exposure to noxious stimuli and against programmed cell death (apoptosis) associated with exposure to inadequate amounts of trophic factors is of great interest in contemporary biology. We have found that N-acetyl-L-cysteine (NAC) is able to promote cell survival in these two distinct experimental paradigms of, respectively, \"death by murder\" and \"death by neglect.\" In the former case, NAC prevented the death of oligodendrocytes induced by glutamate or tumor necrosis factor-alpha (TNF-alpha), and also prevented TNF-alpha-induced death of L929 cells. NAC also acted in synergy with ciliary neurotrophic factor (CNTF) to prevent killing of oligodendrocytes by TNF-alpha. In analysis of \"death by neglect,\" NAC markedly enhanced the extent of spinal ganglion neuron survival obtained with suboptimal concentrations of nerve growth factor and of oligodendrocyte survival obtained with suboptimal concentrations of CNTF or insulin-like growth factor-1. Surprisingly, significant rescue of oligodendrocytes from apoptosis was also observed with combinations of NAC with progesterone, vitamin C, or Trolox, a water-soluble vitamin E analogue, although not with any of these compounds applied individually. These results demonstrate that cocktails of small molecules such as those we have studied may have beneficial effects not predictable from the action of any individual member of the cocktail. In light of the long clinical history of therapeutic use of NAC and the other compounds identified in our studies, we suggest that it may be of interest to examine use of NAC alone, or combinations of NAC with the other small molecules we have studied, in conditions in which certain toxin-mediated forms of cell death or apoptosis contribute significantly to disease.","PeriodicalId":77321,"journal":{"name":"Perspectives on developmental neurobiology","volume":"3 2","pages":"121-31"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19794559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Do central nervous system neurons require target-derived neurotrophic support for survival throughout adult life and aging? 中枢神经系统神经元是否需要目标来源的神经营养支持来维持整个成人生活和衰老?

Perspectives on developmental neurobiology Pub Date : 1996-01-01

C N Svendsen, M V Sofroniew

引用次数: 0

Calcium and Free Radicals: Mediators of neurotrophic factor and excitatory transmitter-regulated developmental plasticity and cell death. 钙和自由基:神经营养因子和兴奋性递质调节的发育可塑性和细胞死亡的介质。

Perspectives on developmental neurobiology Pub Date : 1996-01-01

M P Mattson

{"title":"Calcium and Free Radicals: Mediators of neurotrophic factor and excitatory transmitter-regulated developmental plasticity and cell death.","authors":"M P Mattson","doi":"","DOIUrl":"","url":null,"abstract":"An intricate interplay between neurotrophic factor and excitatory transmitter signaling systems exists in both the developing and adult brain. Interactions between these signaling systems appears to be a fundamental mechanism regulating adaptive neuritic pruning and cell death. Accordingly, genetically and environmentally induced imbalances in this regulatory system are implicated in the pathogenesis of a variety of acute (such as stroke and traumatic brain injury) and chronic (such as Alzheimer's and Parkinson's diseases) neurodegenerative disorders. Neurons exhibit both acute and delayed responses to neurotrophic factors and excitatory transmitters; acute responses include rapid structural remodeling of growth cones and synaptic contacts, and delayed responses include induction or suppression of the expression of gene products involved in neuroprotection. Intracellular free Ca2+ and free radicals appear to play key roles as mediators of both acute and delayed responses of neurons to excitatory transmitters and neurotrophic factors. For example, the delayed response to bFGF includes stabilization of Ca2+ homeostasis and induction of antioxidant enzymes; both of these actions of bFGF antagonize the dendrite outgrowth-stabilizing and excitotoxic actions of glutamate. Intricate regulatory interactions exist between glutamate and neurotrophic factor signaling systems so that glutamate can induce the expression of neurotrophic factors and their receptors, and neurotrophic factors modulate the expression of exitatory transmitter receptors. A novel signaling system that can interact with both glutamate and neurotrophic factor systems is that of the beta-amyloid precursor protein, which appears to play important roles in neuronal plasticity and survival. A working model for the regulation of neuronal survival and connectivity is presented, which considers spatial and temporal constraints on release of, and receptors for, neurotrophic factors and excitatory transmitters.","PeriodicalId":77321,"journal":{"name":"Perspectives on developmental neurobiology","volume":"3 2","pages":"79-91"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19794673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0