In vivo calcium imaging of cerebral cortex in hypoxia-ischemia followed by developmental stage-specific injury in rats

Abstract The parietal area is a part of the cortex that is vulnerable in the rat to hypoxia–ischemia (HI) within the early postnatal period. To investigate the localizing mechanism of this cortical injury, we spatiotemporally detected the cortical intracellular calcium changes, as revealed by a calcium-sensitive fluorescence dye, Rhod 2-AM, during 1 h of HI on postnatal days 7–21 in vivo. The calcium level rose to different levels at different cortical points in all animals within the first 20 min. Over the whole cortical area in the camera field, the changes in three groups significantly differed across time at 30 and 60 min, and a chronic increase appeared at days 7–8. After 3 h of reperfusion, microtubule-associated protein 2 (MAP-2) immunoreactivity confirmed that parietal injury was more serious at day 7, whereas the imaging of calcium distribution did not segregate the injured and uninjured areas. Our in vivo findings in the whole brain structure indicate that the age-specific vulnerability of the parietal cortex injury is affected indirectly by the chronic increase in the late HI phase in the early postnatal period, suggesting that each cortical area differs postnatally with respect to the development of calcium regulation and signal transduction involving neural cell death and/or survival.