54 research outputs found

    Merger rates of dark matter haloes: a comparison between EPS and N-body results

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    We calculate merger rates of dark matter haloes using the Extended Press-Schechter approximation (EPS) for the Spherical Collapse (SC) and the Ellipsoidal Collapse (EC) models. Merger rates have been calculated for masses in the range 1010M⊙h−110^{10}M_{\odot}\mathrm{h}^{-1} to 1014M⊙h−110^{14}M_{\odot}\mathrm{h}^{-1} and for redshifts zz in the range 0 to 3 and they have been compared with merger rates that have been proposed by other authors as fits to the results of N-body simulations. The detailed comparison presented here shows that the agreement between the analytical models and N-body simulations depends crucially on the mass of the descendant halo. For some range of masses and redshifts either SC or EC models approximate satisfactory the results of N-body simulations but for other cases both models are less satisfactory or even bad approximations. We showed, by studying the parameters of the problem that a disagreement --if it appears-- does not depend on the values of the parameters but on the kind of the particular solution used for the distribution of progenitors or on the nature of EPS methods. Further studies could help to improve our understanding about the physical processes during the formation of dark matter haloes.Comment: 29 pages, 9 figure

    Localization of Cacna1s to ON Bipolar Dendritic Tips Requires mGluR6-Related Cascade Elements

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    Citation: Tummala SR, Neinstein A, Fina ME, Dhingra A, Vardi N. Localization of Cacna1s to ON bipolar dendritic tips requires mGluR6-related cascade elements. Invest Ophthalmol Vis Sci. 2014;55:148355: -149255: . DOI:10.1167 PURPOSE. L-type voltage gated calcium channels in retina localize primarily at the presynaptic active zones of photoreceptors and bipolar cells where they modulate glutamate release. However, the pore forming subunit Cacna1s of certain L-type channels is also expressed postsynaptically at the tips of ON bipolar cell dendrites where it colocalizes with mGluR6, but has an unknown function. At these dendritic tips, the components of the mGluR6 signaling cascade cluster together in a macromolecular complex, and each one's localization often depends on that of the others. Thus, we explored if Cacna1s is part of the mGluR6 complex. METHODS. We determined Cacna1s expression by PCR using an ON bipolar library, by Western blotting, and by standard immunohistochemistry. RESULTS. The PCR amplification confirmed expression of the transcript in ON bipolar cells, and Western blotting showed the expected bands. Immunostaining for Cacna1s was stronger in the dendritic tips of rod bipolar cells than in those of ON cone bipolar cells. This staining severely decreased in mice missing various mGluR6 cascade elements (Grm6 À/À , Gnao1 À/À , Gnb3 À/À , Gng13 À/À , and Trpm1 À/À ). During development, the ratio of the number of Cacna1s puncta to the number of presynaptic ribbons followed a sigmoidal pattern, rising rapidly from P13 to P17. The mGluR6 expression preceded that of Cacna1s and RGS11. CONCLUSIONS. Our results show that the localization and stability of Cacna1s depend on the expression of mGluR6 and its cascade components, and they suggest that Cacna1s is part of the mGluR6 complex. We hypothesize that Cacna1s contributes to light adaptation by permeating calcium

    Localization of Cacna1s to ON Bipolar Dendritic Tips Requires mGluR6-Related Cascade Elements

    No full text
    PURPOSE. L-type voltage gated calcium channels in retina localize primarily at the presynaptic active zones of photoreceptors and bipolar cells where they modulate glutamate release. However, the pore forming subunit Cacna1s of certain L-type channels is also expressed postsynaptically at the tips of ON bipolar cell dendrites where it colocalizes with mGluR6, but has an unknown function. At these dendritic tips, the components of the mGluR6 signaling cascade cluster together in a macromolecular complex, and each one's localization often depends on that of the others. Thus, we explored if Cacna1s is part of the mGluR6 complex. METHODS. We determined Cacna1s expression by PCR using an ON bipolar library, by Western blotting, and by standard immunohistochemistry. RESULTS. The PCR amplification confirmed expression of the transcript in ON bipolar cells, and Western blotting showed the expected bands. Immunostaining for Cacna1s was stronger in the dendritic tips of rod bipolar cells than in those of ON cone bipolar cells. This staining severely decreased in mice missing various mGluR6 cascade elements (Grm6(−/−), Gnao1(−/−), Gnb3(−/−), Gng13(−/−), and Trpm1(−/−)). During development, the ratio of the number of Cacna1s puncta to the number of presynaptic ribbons followed a sigmoidal pattern, rising rapidly from P13 to P17. The mGluR6 expression preceded that of Cacna1s and RGS11. CONCLUSIONS. Our results show that the localization and stability of Cacna1s depend on the expression of mGluR6 and its cascade components, and they suggest that Cacna1s is part of the mGluR6 complex. We hypothesize that Cacna1s contributes to light adaptation by permeating calcium
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