Abstract
BackgroundThe neuroprotective effect of xenon has been demonstrated for glutamatergic neurons. In the present study it is investigated if dopaminergic neurons, i.e. nerve-growth-factor differentiated PC-12 cells, are protected as well against hypoxia-induced cell damage in the presence of xenon.ResultsPheochromocytoma cells differentiated by addition of nerve growth factor were placed in a N2-saturated atmosphere, a treatment that induced release of dopamine, reaching a maximum after 30 min. By determining extracellular lactate dehydrogenase concentration as marker for concomitant cellular damage, a substantial increase of enzymatic activity was found for N2-treated cells. Replacement of N2 by xenon in such a hypoxic atmosphere resulted in complete protection against cellular damage and prevention of hypoxia-induced dopamine release. Intracellular buffering of Ca2+ using the Ca-chelator 1, 2-bis(2-Aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis(acetoxymethyl) ester (BAPTA) reduced the neuroprotective effect of xenon indicating the essential participation of intracellular Ca2+-ions in the process of xenon-induced neuroprotection.ConclusionsThe results presented demonstrate the outstanding property of xenon to protect neuron-like cells in a hypoxic situation.
Highlights
The neuroprotective effect of xenon has been demonstrated for glutamatergic neurons
In recent years several lines of evidence have suggested that effects other than excitotoxic mechanisms may participate in hypoxiainduced cell damage such as cortical spreading depression [7,8]
They were kept in an atmosphere consisting of 100% nitrogene, considerable amounts of dopamine were found in the extracellular space reaching a maximum at 30 min of incubation, followed by a subsequent decrease
Summary
In the present study it is investigated if dopaminergic neurons, i.e. nerve-growth-factor differentiated PC-12 cells, are protected as well against hypoxia-induced cell damage in the presence of xenon. Rat pheochromocytoma (PC-12) cells are catecholaminergic, excitable cells that have been widely used as an in vitro model for neuronal cells [9] possessing both D1- and D2-dopamine receptors [10]. In these cells hypoxia causes a transient release of dopamine resulting from a complex cellular response consisting of increased dopamine release and reduced uptake rate.
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