Transient oxygen–glucose deprivation causes immediate changes in redox activity in mouse brain tissue

Redox activity is an important property of living cells, and decreases in redox activity are likely to be an upstream event in ischemic brain injuries. In this study, immediate changes in redox activity caused by ischemic injury were investigated in oxygen–glucose deprivation (OGD) treated mouse brain tissue. Adult mouse brain slices were subjected to 10 min or 15 min OGD treatments and were immediately stained with an MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) staining procedure. After 10 min OGD, the redox activity decreased in the lateral globus pallidus (LGP), medial globus pallidus (MGP), pyramidal cell layer of hippocampus CA1 (CA1PL) and the granular layer of the cerebellum (cerebGL). After 15 min OGD, decreases also occurred in the substantia nigra (SN) and several other areas of the brain stem. Hoechst 33342 was used to confirm that changes in redox activity occurred before morphological alterations in the cellular nuclei — morphological changes were not observed even after a 60 min OGD. The results presented here indicate that functional ischemic vulnerability exists in several brain regions, and will be helpful for systematic research on mammalian brain injury caused by transient metabolic stress.

Research highlights
► Mouse brain tissues were tested immediately by MTT staining following transient OGD.
► Decreases in redox activity were evident especially in several basal ganglia nuclei.
► Morphological changes in cellular nuclei not occurred following the OGD treatment.