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  • 1
    Electronic Resource
    Electronic Resource
    Differential induction of NF-κB activity and neural cell death by antidepressants in vitro (2000)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 12 (2000), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Tricyclic antidepressants and selective serotonin reuptake inhibitors are here shown to induce cell death in a neural cell line. The exposure to these drugs led to increased generation of reactive oxygen species and a concomitant reduction of intracellular glutathione levels. Furthermore, these antidepressants induced DNA fragmentation and increased the transcriptional and DNA-binding activity of NF-κB. In contrast, treatment with type A and B monoamine oxidase inhibitors did not induce changes in NF-κB activity and did not exert a detrimental influence on cell viability. These results indicate that some antidepressant drugs may cause both oxidative stress and changes in cellular antioxidative capacity, resulting in altered NF-κB activity and, ultimately, cell death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.0953-816X.2000.01352.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Repetitive transcranial magnetic stimulation in rats: evidence for a neuroprotective effect in vitro and in vivo (1999)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 11 (1999), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In recent years, repetitive transcranial magnetic stimulation (rTMS) of the human brain has been used as a therapeutic tool in a variety of psychiatric and neurological disorders. However, to understand the mechanisms underlying any potential therapeutic effects, and possible adverse effects, studies are necessary on how magnetic stimuli induced by rTMS interact with central nervous system (CNS) regulation. In the current study, we failed to find cognitive impairments or structural alterations in rat brains after 11 weeks of long-term treatment with rTMS, which if present would indicate neuronal damage. In contrast, our in vitro studies showed that magnetic stimulation analogous to rTMS increased the overall viability of mouse monoclonal hippocampal HT22 cells and had a neuroprotective effect against oxidative stressors, e.g. amyloid beta (Aβ) and glutamate. The treatment increased the release of secreted amyloid precursor protein (sAPP) into the supernatant of HT22 cells and into cerebrospinal fluid from rats. HT22 cells preincubated with cerebrospinal fluid from rTMS-treated rats were found to be protected against Aβ. These findings suggest that neurochemical effects induced by rTMS do not lead to reduced neuronal viability, and may even reduce the detrimental effects of oxidative stress in neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.1999.00747.x
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Expression of synaptophysin in sprouting neurons after entorhinal lesion in the rat (1997)
    Springer
    Experimental brain research 117 (1997), S. 80-86 
    Details
    ISSN: 1432-1106
    Keywords: Key words Hippocampus ; Commissural fibers ; Reactive sprouting ; Synaptogenesis ; Synaptophysin ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Expression of the synaptic vesicle protein synaptophysin was studied in lesion-induced sprouting neurons of the contralateral entorhinal cortex and in the contralateral dentate gyrus using immunocytochemistry at the light- and electron-microscopic level. Perikaryal immunoreactivity for synaptophysin was found between 8 and 10 days postlesion. Light microscopy revealed that synaptophysin immunostaining was present in almost all neurons of layers II and III of the contralateral medial entorhinal cortex. These neurons give rise to the sprouting, crossed temporodentate pathway. In addition, some hilar neurons of the contralateral dentate gyrus, which are the parent cells of sprouting commissural fibers, were immunostained for synaptophysin. Transient immunostaining for synaptophysin was observed within cell bodies and dendrites. Additionally, the cell bodies were outlined by immunoreactive puncta, identified by electron microscopy as nerve terminals. Our results revealed that sprouting neurons express the major synaptic vesicle protein synaptophysin during reactive synaptogenesis in a pattern that reflects biosynthesis and sorting of this protein as seen in developing neurons during synapse formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002210050201
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    Paper (German National Licenses)
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