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  • 1
    Electronic Resource
    Electronic Resource
    Role of Synaptophysin in Exocytotic Release of Dopamine from Xenopus Oocytes Injected with Rat Brain mRNA (2000)
    Springer
    Cellular and molecular neurobiology 20 (2000), S. 401-408 
    Details
    ISSN: 1573-6830
    Keywords: synaptophysin ; dopamine release ; Xenopus oocyte ; rat brain mRNA ; exocytosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract 1. The role of synaptophysin in the exocytotic release of dopamine (DA) was examined in Xenopus laevis oocytes injected with rat brain mRNA. 2. The mRNA-injected oocytes showed DA uptake which depended on the incubation time and external DA concentrations. 3. Stimulation with KCl (10–50 mM) of mRNA-injected oocytes preloaded with DA evoked external Ca2+-dependent release of DA. The noninjected and water-injected oocytes did not produce uptake of DA and stimulation-evoked release of DA. 4. The high-KCl (50 mM)-stimulated release of DA decreased in the oocytes injected with rat brain mRNA together with antibody to synaptophysin. 5. Immunoblot analysis demonstrated that synaptophysin was expressed in the brain mRNA-injected oocytes but not in the noninjected and water-injected oocytes. 6. Thus, uptake and release machinery similar to native dopaminergic nerve terminals was expressed in Xenopus oocytes by injecting mRNA-extracted from the rat brain, and synaptophysin may play a role in the exocytotic release of DA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007022428041
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  • 2
    Electronic Resource
    Electronic Resource
    Involvement of Glial Cells in Cyclosporine-Increased Permeability of Brain Endothelial Cells (2000)
    Springer
    Cellular and molecular neurobiology 20 (2000), S. 781-786 
    Details
    ISSN: 1573-6830
    Keywords: cyclosporine ; neurotoxicity ; glia@keyword = blood–brain barrier
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract SUMMARY 1. To test whether astrocytes participate in cyclosporine-induced dysfunction of the blood-brain barrier, we examined the effects of cyclosporine on the permeability of the mouse brain endothelial (MBEC4) cells cocultured with C6 glioma cells, each cell layer placed on the top and bottom of the insert membrane, respectively. 2. The presence of C6 cells remarkably aggravated cyclosporine-increased permeability of MBEC4 cells to sodium fluorescein. 3. In light of these findings, the possibility that astroglial cells could contribute to the occurrence of cyclosporine-induced dysfunction of the blood-brain barrier triggering neurotoxicity should be considered.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007015228318
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Involvement of Glial Endothelin/Nitric Oxide in Delayed Neuronal Death of Rat Hippocampus After Transient Forebrain Ischemia (2000)
    Springer
    Cellular and molecular neurobiology 20 (2000), S. 541-551 
    Details
    ISSN: 1573-6830
    Keywords: nitric oxide synthase ; endothelin ETB receptor ; microglia, astrocytes ; delayed neuronal death ; transient forebrain ischemia ; hippocampus CA1 subfield (rat)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract 1. We examined time- and cell-type-dependent changes in endothelin (ET)-1-like immunoreactivity, ET receptors binding and nitric oxide (NO) synthase (NOS) activity in CA1 subfields of the hippocampus of stroke-prone spontaneously hypertensive rats subjected to a 10-min bilateral carotid occlusion and reperfusion. 2. Microglia aggregated in accord with neuronal death and expressed a high density of ETB receptors and an intense NOS activity in the damaged CA1 pyramidal cell layer, 7 days after the induced transient forebrain ischemia. The increased NOS activity and ETB receptor in microglia disappeared 28 days after this transient ischemia. 3. In contrast to microglia, astrocytes presented a moderate level of ET-1-like immunoreactivity, ETB receptors, and NOS activity in all areas of the damaged CA1 subfields, 7 days after the ischemia. These events were further enhanced 28 days after the ischemia. 4. In light of these findings, the possibility that the microglial and the astrocytic ETB/NO system largely contributes to development of the neuronal death and to reconstitution of the damaged neuronal tissue, respectively, in the hippocampus subjected to a transient forebrain ischemia would have to be considered.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007007710703
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    Paper (German National Licenses)
    Fulltext
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