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Seven\u2010day\u2010old rats were induced with H\u2010I injury, and scanned for <jats:italic>T<\/jats:italic><jats:sub>1<\/jats:sub>\u2010weighted image (<jats:italic>T<\/jats:italic><jats:sub>1<\/jats:sub>WI) and <jats:italic>T<\/jats:italic><jats:sub>2<\/jats:sub>\u2010weighted image (<jats:italic>T<\/jats:italic><jats:sub>2<\/jats:sub>WI) with and without systemic MnCl<jats:sub>2<\/jats:sub> administration. Serial histological analysis was performed for Mn\u2010superoxide dismutase (Mn\u2010SOD) and glutamine synthetase (GS), which are Mn\u2010binding enzymes against the oxidative stress and glutamate excitotoxicity in neurodegeneration. In the acute phase (first 2 days), the ipsilateral lesion exhibited no Mn enhancement in <jats:italic>T<\/jats:italic><jats:sub>1<\/jats:sub>WIs, with histology showing no Mn\u2010SOD and GS production. In the mid\u2010phase (from day 3), Mn enhancement was found in the cortex, basal ganglia, and hippocampus, correlating with local Mn\u2010SOD and GS increase. In the late phase, the enhancement became more localized to the pericyst basal ganglia and cortex, and then gradually diminished. In <jats:italic>T<\/jats:italic><jats:sub>2<\/jats:sub>WIs, a signal decrease was observed from day 3 in the corresponding regions. Hypointense voids gradually formed in the late phase, correlating with the local iron accumulation. H\u2010I rats without Mn<jats:sup>2+<\/jats:sup> administration exhibited similar but weak changes in <jats:italic>T<\/jats:italic><jats:sub>1<\/jats:sub>WIs and <jats:italic>T<\/jats:italic><jats:sub>2<\/jats:sub>WIs from days 14 and 7, respectively. These results indicate that Mn<jats:sup>2+<\/jats:sup> may be a useful in vivo probe for monitoring Mn\u2010SOD and GS enzymatic activities. 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