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Mammalian Nervous System (mammalian + nervous_system)
Selected AbstractsFORMS OF PLASTICITY IN THE MAMMALIAN NERVOUS SYSTEMPSYCHOPHYSIOLOGY, Issue S1 2005Article first published online: 15 AUG 200 No abstract is available for this article. [source] Characterization of the expression of PDZ-RhoGEF, LARG and G,12/G,13 proteins in the murine nervous systemEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2002R. Kuner Small GTPases of the Rho-family, like Rho, Rac and Cdc42, are involved in neuronal morphogenesis by regulating growth cone morphology or dendritic spine formation. G-proteins of the G12 -family, G12 and G13, couple G-protein-coupled receptors (GPCRs) to the activation of RhoA. Recently, two novel Rho-specific guanine nucleotide exchange factors (RhoGEFs), PDZ-RhoGEF and LARG, have been identified to interact with the activated ,-subunits of G12/G13 and are thus believed to mediate GPCR-induced Rho activation. Although studies in neuronal cell lines have shown that G12/G13 and PDZ-RhoGEF mediate GPCR-induced neurite retraction, the role, as well as the expression of this signalling pathway, in intact brain has not been adequately studied. In the present study, we have characterized systematically the expression of G,12, G,13, PDZ-RhoGEF and LARG in various murine tissues as well as their subcellular localization in the central and peripheral nervous systems. By performing immunohistochemistry, using polyclonal antibodies raised against the above proteins, we observed that G,12, G,13 and their RhoGEF-effectors are distributed widely in the mammalian nervous system. Moreover, these proteins localize to distinct morphological compartments within neurons. While LARG and G,12 were mainly found in somata of the neurons, PDZ-RhoGEF and G,13 were predominantly localized in the neuropil of central neurons. Interestingly, PDZ-RhoGEF is a neural-specific protein, whereas LARG is nearly ubiqoutous. Our data provide evidence that the G12/13,RhoGEF-mediated pathway is present throughout the adult brain and may be involved in regulation of neuronal morphogenesis and function via GPCRs. [source] Developmental and adult expression of semaphorin 2a in the cricket Gryllus bimaculatus,THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2007Kristen R. Maynard Abstract Developmental guidance cues act to direct growth cones to their correct targets in the nervous system. Recent experiments also demonstrate that developmental cues are expressed in the adult mammalian nervous system, although their function in the brain is not yet clear. The semaphorin gene family has been implicated in the growth of dendrites and axons in a number of different species. While the expression of semaphorin and its influence on tibial pioneer neurons in the developing limb bud have been well characterized in the grasshopper, the expression of semaphorin 2a (sema2a) has not been explored in the adult insect. In this study we used polymerase chain reaction (PCR) with degenerate and gene-specific primers to clone part of the secreted form of sema2a from Gryllus bimaculatus. Using in situ hybridization and immunohistochemistry, we confirmed that sema2a mRNA and protein expression patterns in the embryonic cricket were similar to that seen in the grasshopper. We also showed that tibial neuron development in crickets was comparable to that described in grasshopper. An examination of both developing and adult cricket brains showed that sema2a mRNA and protein were expressed in the Kenyon cells in mushroom bodies, an area involved in learning and memory. Sema2a expression was most obvious near the apex of the mushroom body in a region surrounding the neurogenic tip, which produces neurons throughout the life of the cricket. We discuss the role of neurogenesis in learning and memory and the potential involvement of semaphorin in this process. J. Comp. Neurol. 503:169,181, 2007. © 2007 Wiley-Liss, Inc. [source] Transitin, a nestin-related intermediate filament, is expressed by neural progenitors and can be induced in Müller glia in the chicken retinaTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2005Andy J. Fischer Abstract The purpose of this study was to test whether transitin, the avian homologue of nestin, is expressed by retinal progenitors in the developing and postnatal chicken. Because nestin has been widely used as a cell-distinguishing marker of neural progenitors in the mammalian nervous system, we expected to find transitin expressed specifically by the neural progenitors of the retina. In early stages of development, transitin is expressed by neural progenitors in the retina and by cells in the developing ciliary body. During later stages of development, transitin expression persists in differentiating Müller glia but is down-regulated by these cells as maturation proceeds. In the postnatal chick, transitin expression is restricted to neural progenitors at the peripheral edge of the retina. We found that the expression of transitin in mature Müller glia was induced by intraocular injections of insulin and fibroblast growth factor-2 (FGF2) but not by ciliary neurotrophic factor. In response to insulin and FGF2, the expression of transitin was induced in the nonpigmented epithelium (NPE) of the ciliary body. In the postnatal retina, acute retinal damage transiently induces transitin expression in Müller glia. We propose that the expression of transitin by retinal Müller glia and NPE cells in the postnatal animal represents a state of de-differentiation and a step toward becoming neurogenic progenitor cells. Taken together, our findings indicate that transitin is expressed by neural progenitors in the embryonic and postnatal chicken retina. However, transitin is not exclusively expressed by neural progenitors and is also expressed by non-neurogenic cells. J. Comp. Neurol. 484:1,14, 2005. © 2005 Wiley-Liss, Inc. [source] False resurrections: Distinguishing regenerated from spared axons in the injured central nervous systemTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2003Oswald Steward Abstract Several recent studies report that axon regeneration can be induced in the mature mammalian nervous system by novel treatments or genetic manipulations. In assessing these reports, it is important to be mindful of the history of regeneration research, which is littered with the corpses of studies that reported regeneration that later proved incorrect. One important reason is the "spared axon conundrum," in which axons that survive a lesion are mistakenly identified as having regenerated. Here, we illustrate the problem and propose criteria that may be used to identify regenerated vs. spared axons, focusing on the injured spinal cord. J. Comp. Neurol. 459:1,8, 2003. © 2003 Wiley-Liss, Inc. [source] | ||||||||||