Astrocytes in the brain migrate to sites of injury where they can take up damaging molecules extruded from injured cells to protect neurons. The astrocytic response to cell death is critical to our understanding of ways to mitigate secondary injury from a traumatic brain injury(TBI). We previously showed that a laser could be used to induce a single cell death (photolysis) in order to monitor the surrounding astrocytic response. We found that photolysis leads to a calcium transient in surrounding astrocytes. Here we show that cells treated with the internal calcium chelator BAPTA-AM do not exhibit a transient. Similarly, cells whose endoplasmic reticulum (ER) has been depleted through blocking of the SERCA pump do not show a calcium increase. Cells treated with EGTA to chelate external calcium showed no statistical significance when compared to cells in regular medium with calcium. Therefore, it is concluded that the ER stores are largely responsible for the cytosolic calcium transient.
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