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. Author manuscript; available in PMC: 2013 Jan 1.
Published in final edited form as: J Neuroendocrinol. 2012 Jan;24(1):236–248. doi: 10.1111/j.1365-2826.2011.02251.x

Figure 7. SERMs increased mitochondrial respiration in vitro.

Figure 7

A. Primary rat embryonic (E18) neurones from hippocampus were cultured for 10 days in Neurobasal Media with B27 supplement and then treated with E2 (10 ng/ml), PPT (100 ng/ml), or DPN (100 ng/ml) or vehicle for 24 h prior to the experiment. Oxygen consumption rates (OCR) were determined using Seahorse XF-24 Metabolic Flux Analyzer. Vertical lines indicate time of addition of mitochondrial inhibitors A: oligomycin (1 μM), B: FCCP (1 μM) or C: rotenone (1 μM). OCR in primary neurones treated with E2 (10 ng/ml) and DPN (100 ng/ml) exhibited a greater magnitude of maximal mitochondrial respiratory capacity compared to vehicle (*=P<0.05 vs. vehicle; n=4). Primary rat embryonic (E18) mixed glia from hippocampus were cultured for 14 days in DMEM supplemented with 10% serum. B. Glial cells derived from primary rat embryonic (E18) hippocampus were cultured for 10 days before re-plating. Mixed glial cells were serum-starved 4 h then treated with E2 (10 ng/ml), PPT (100 ng/ml), DPN (100 ng/ml) or vehicle for 24 h prior to the experiment. Vertical lines indicate time of addition of mitochondrial inhibitors A: oligomycin (1 μM), B: FCCP (1 μM) or C: rotenone (1 μM). OCR in primary glia treated with E2 (10 ng/ml), PPT (100 ng/ml), or DPN (100 ng/ml) displayed greater basal respiration and increased maximal mitochondrial respiratory capacity compared to vehicle (*=P<0.05 vs. vehicle; n=4).