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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Applied physics 45 (1988), S. 37-44 
    ISSN: 1432-0649
    Keywords: 42.65 ; 78.30j
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract Several theoretical and numerical models have been published which describe the evolution of a Stokes beam in a Raman medium excited by a focussed pump beam. Generally, the published theoretical departures from the plane-wave theory of Raman scattering are based on assumptions about the power of the pump beam. In this paper we present a theoretical model which is shown to be in excellent agreement with an exact numerical treatment, and which is valid without restrictions on the pump power. Its predictions are used to indicate the range of validity of earlier theories.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-6903
    Keywords: Hepatic encephalopathy ; brain slices ; striatum ; frontal cortex ; glutamate receptors ; dopamine release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of depolarizing stimuli; high (50 mM) potassium ions and the glutamate receptor agonists N-methyl-D-aspartate, kainate and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) on the release of newly-loaded [3H]dopamine were studied in frontal cortical and striatal slices from control rats and from rats with acute hepatic encephalopathy induced with a hepatotoxin, thioacetamide. Hepatic encephalopathy enhanced the stimulatory effect of potassium ions by 20% in striatal slices and by 34% in frontal cortical slices. In striatal slices the stimulatory effects of N-methyl-D-aspartate and kainate were depressed in hepatic encephalopathy by 46% and 21%, respectively, which may be taken to reflect impaired modulation of striatal dopamine release by glutamate acting at N-methyl-D-aspartate or kainate receptors. In frontal cortical slices, the stimulatory effect of kainate was enhanced by 35% in hepatic encephalopathy but N-methyl-D-aspartate-stimulated release was not affected. The release evoked by 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate was not affected in hepatic encephalopathy in either brain region. Stimulation of dopamine release in the frontal cortex by depolarization or glutamate acting at kainate receptors could inhibit the activity of descending corticostriatal glutamatergic pathways, further impairing regulation of dopamine release by glutamate in the stratum.
    Type of Medium: Electronic Resource
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