{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T11:28:17Z","timestamp":1769167697978,"version":"3.49.0"},"reference-count":39,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":334,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2008,3]]},"abstract":"<jats:sec><jats:title>Background and purpose:<\/jats:title><jats:p>Reactive oxygen species (ROS) have been postulated to play a crucial role in the pathogenesis of ischaemia\u2010reperfusion injury. Among these, hydrogen peroxide (H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>) is known to be a toxic compound responsible for free\u2010radical\u2010dependent neuronal damage. In recent years, however, the \u2018bad reputation\u2019 of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> and other ROS molecules has changed. The aim of this study was to assess the protective role of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> and modification in its endogenous production on the electrophysiological and morphological changes induced by oxygen\/glucose deprivation (OGD) on CA1 hippocampal neurons.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental approach:<\/jats:title><jats:p>Neuroprotective effects of exogenous and endogenous H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> were determined using extracellular electrophysiological recordings of field excitatory post synaptic potentials (fEPSPs) and morphological studies in a hippocampal slice preparation. <jats:italic>In vitro<\/jats:italic> OGD was delivered by switching to an artificial cerebrospinal fluid solution with no glucose and with oxygen replaced by nitrogen.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key results:<\/jats:title><jats:p>Neuroprotection against <jats:italic>in vitro<\/jats:italic> OGD was observed in slices treated with H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> (3 mM). The rescuing action of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> was mediated by catalase as pre\u2010treatment with the catalase inhibitor 3\u2010amino\u20101,2,4\u2010triazole blocked this effect. More interestingly, we showed that an increase of the endogenous levels of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>, due to a combination of an inhibitor of the glutathione peroxidase enzyme and addition of Cu,Zn\u2010superoxide dismutase in the tissue bath, prevented the OGD\u2010induced irreversible depression of fEPSPs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and implications:<\/jats:title><jats:p>Taken together, our results suggest new possible strategies to lessen the damage produced by a transient brain ischaemia by increasing the endogenous tissue level of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>.<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2008) <jats:bold>153<\/jats:bold>, 1022\u20131029; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0707587\">10.1038\/sj.bjp.0707587<\/jats:ext-link>; published online 28 January 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