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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.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Results<\/jats:title>\n                        <jats:p>Pheochromocytoma cells differentiated by addition of nerve growth factor were placed in a N<jats:sub>2<\/jats:sub>-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 N<jats:sub>2<\/jats:sub>-treated cells. Replacement of N<jats:sub>2<\/jats:sub> by xenon in such a hypoxic atmosphere resulted in complete protection against cellular damage and prevention of hypoxia-induced dopamine release. Intracellular buffering of Ca<jats:sup>2+<\/jats:sup> using the Ca-chelator 1, 2-<jats:italic>bis<\/jats:italic>(2-Aminophenoxy)ethane-N,N,N',N'-tetraacetic acid <jats:italic>tetrakis<\/jats:italic>(acetoxymethyl) ester (BAPTA) reduced the neuroprotective effect of xenon indicating the essential participation of intracellular Ca<jats:sup>2+<\/jats:sup>-ions in the process of xenon-induced neuroprotection.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Conclusions<\/jats:title>\n                        <jats:p>The results presented demonstrate the outstanding property of xenon to protect neuron-like cells in a hypoxic situation.<\/jats:p>\n                     <\/jats:sec>","DOI":"10.1186\/1471-2202-5-55","type":"journal-article","created":{"date-parts":[[2005,1,12]],"date-time":"2005-01-12T16:05:43Z","timestamp":1105545943000},"update-policy":"http:\/\/dx.doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Xenon prevents cellular damage in differentiated PC-12 cells exposed to hypoxia"],"prefix":"10.1186","volume":"5","author":[{"given":"Christian","family":"Petzelt","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Per","family":"Blom","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wolfgang","family":"Schmehl","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jana","family":"M\u00fcller","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wolfgang J","family":"Kox","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2004,12,8]]},"reference":[{"key":"131_CR1","doi-asserted-by":"crossref","first-page":"431","DOI":"10.1152\/physrev.1999.79.4.1431","volume":"79","author":"P Lipton","year":"1999","unstructured":"Lipton P: Ischemic cell death in brain neurons. 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