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    Determination of NADH by laser-induced fluorescence spectroscopy: applications in preclinical neuroscience (2007)

    Art
    Poster
    Autoren
    Rex, A.
    Hamann, M.
    Richter, A.
    Fink, F.
    Fink, H.
    Kongress
    48th Spring Meeting Deutsche Gesellschaft für Experimentelle und Klinische Pharmakologie und Toxikologie
    Mainz, 13. – 15.03.2007
    Quelle
    Naunyn-Schmiedeberg´s Archives of Pharmacology; 375(Suppl 1) — S. 57
    ISSN: 0028-1298
    Sprache
    Englisch
    Kontakt
    Institut für Pharmakologie und Toxikologie

    Koserstr. 20
    14195 Berlin
    Tel.+49 30 838 53221 Fax.+49 30 838 53112
    email:pharmakologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    There is an increasing need for continuously monitoring changes in brain metabolism
    and neuronal activity, respectively. The majority of the energy, which is produced in
    neurons, is necessary for the maintenance of the physiological neuronal activity. The
    extent of the energy production is thus closely coupled to the neural activity.
    Measurement of NAD(P)H fluorescence by laser-induced fluorescence spectroscopy
    and with small glass fibre probes allows the determination of the mitochondrial activity,
    and therefore neuronal activity indirectly, in the brain with high temporal and spatial
    resolution (Rex & Fink, 2006, Las.Phys.Lett.,3:452-9). In vitro, dependence between the
    NADH concentration and NADH fluorescence was proven. Ex vivo investigations
    showed that under the selected spectroscopic conditions predominantly NADH
    fluorescence contributes to the fluorescence of the tissue and that the fluorescence
    intensity differs between brain regions. We could show in anaesthetized rats that the
    fluorescence intensity of NADH in the cortex is inversely proportional to the metabolic
    activity and that changes in the NADH fluorescence due to haemodynamical effects
    altering the optical properties of the tissue can be excluded. In further in vivo
    experiments administration of a serotonin 1A receptor agonist with known anxiolytic
    activity and inhibitory effects on neuronal activity in the hippocampus causes a
    reversible increase in the intensity of hippocampal NADH fluorescence in
    pharmacologically relevant doses. In awake and freely moving mutant dtsz hamsters, a
    model of paroxysmal dystonia, we could measure reversible changes of the NADH
    fluorescence during a dystonic episode. The magnitude of the change corresponds to
    the severity of the dystonic episode. The laser-induced fluorescence spectroscopy of the
    intrinsic and mainly mitochondrial bound NADH is a versatile applicable and reliable
    method which allows the spatial and temporal characterization of the metabolic state
    and thus the neuronal activity in the brain in vitro and in vivo