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. Author manuscript; available in PMC: 2017 Jun 21.
Published in final edited form as: Ann N Y Acad Sci. 2016 Jun 21;1374(1):176–183. doi: 10.1111/nyas.13122

Figure 1.

Figure 1

Development of Ca2+ plateau and its mechanism following OP-induced SE. (A) Hippocampal CA1 [Ca2+]i from age-matched control (white bar) and POX-exposed rats were isolated 1 h and 1, 7, and 30 days after SE (black bars). [Ca2+]i in POX-SE rats was significantly higher than control values at all the time points and did not return to baseline, even at 30 days post-SE (Ca2+ plateau). (B) Hippocampal CA1 [Ca2+]i from control rats (white bar), DFP-treated rats (black bar), and DFP + MK-801–treated rats (grey bars) were isolated 1 -h after SE. MK-801 pretreatment prevented the elevations in [Ca2+]i that occur following DFP-induced SE. However, MK-801 treatment 1 h after DFP-induced SE did not significantly affect DFP-SE induced [Ca2+]i elevations. (C)Hippocampal CA1 [Ca2+]i from control rats (white bar), POX-treated rats (black bars), and POX + drugs rats (grey bars) were isolated 48 h after SE. [Ca2+]i in neurons isolated from POX-SE rats treated with either dantrolene (DANT), levetiracetam (LEV), or carisbamate (CRB) were significantly lower than POX SE rats (no drugs) values at the respective time point. All data represented as mean ± SEM. *P < 0.05 Data in 1A and 1C reproduced from Ref. 14, with permission.