In the present study, we observed chronological changes of
antioxidant-like
protein 1 (AOP-1) in the gerbil hippocampal CA1 region after 5 min of transient forebrain
ischemia using immunohistochemistry and western blot. AOP-1 was significantly altered in the CA1 region after transient
ischemia. In the
sham-operated group, AOP-1 immunoreactivity was detected in pyramidal and non-pyramidal cells of the CA1 region. At 30 min after ischemic insult, AOP-1 immunoreactivity and
protein level was decreased in the CA1 region. At 12 h after ischemic insult, AOP-1 immunoreactivity and
protein level was highest in this region. At this time, after
ischemia, AOP-1 immunoreactivity in non-pyramidal cells was high compared to the
sham-operated group. Based on double immunofluorescence study, AOP-1-immunoreactive neurons were identified as GABAergic, which were stained with GAD or
parvalbumin. Thereafter, AOP-1 immunoreactivity and
protein levels were decreased time-dependently. From 4 days after ischemic insult, AOP 1 immunoreactivity was generally expressed in astrocytes. Five days after ischemic insult, AOP-1 immunoreactivity and
protein level was increased again to 1.4 folds compared to that of the
sham-operated group. In brief, AOP-1 immunoreactivity was increased in GABAergic non-pyramidal cells in the hippocampal CA1 region at early time after ischemic insult and was expressed in astrocytes at late time after
ischemia. This result suggests that AOP-1 may be important role in homeostasis of GABAergic neurons because these neurons are resistant to ischemic damage.