Skip to main content
. Author manuscript; available in PMC: 2010 Apr 21.
Published in final edited form as: Neuroscience. 2009 Feb 13;160(1):51–60. doi: 10.1016/j.neuroscience.2009.02.013

Fig. 3.

Fig. 3

Source of increased [Ca2+]i during preconditioning hypoxia is intracellular stores. A. [Ca2+]i in CA1 neurons during hypoxic preconditioning in untreated control slices, and in slices pre-treated with a phospholipase C inhibitor (U73122, 1 μM), an IP3 receptor antagonist xestospongin C (xesto C. 1 μM), the NMDA receptor antagonist a-phosphonovalerate (APV, 10 μM) or low extracellular Ca2+ (<0.1 mM). Data are means ±SEM in 8–10 slices. B. Depletion of [Ca2+]i stores with thapsigargin (10 μM) decreases the magnitude of the [Ca2+]I rise in CA1 during hypoxia. * indicates significant (P<0.05) increase in [Ca2+]i compared to hypoxia alone group. Data are means±SD for 6 experiments.