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. 2007 Nov 26;153(3):598–608. doi: 10.1038/sj.bjp.0707597

Figure 5.

Figure 5

Effects of coapplication of eupalmerin acetate (EPA) and steroids. (a) The effect of the specific steroid antagonist (3α,5α)-17-phenylandrost-16-en-3-ol (17-PA) on potentiation elicited by EPA. The cell was exposed to 0.5 μM GABA, GABA+30 μM EPA or GABA+EPA+10 μM 17-PA. The presence of 17-PA reduced the potentiating effect of EPA, suggesting that EPA acts on the receptor through the steroid site. The peak amplitudes were 163 pA (GABA alone), 344 pA (GABA+EPA) and 220 pA (GABA+EPA+17-PA). The averaged values from all experiments are given in the text. (b) The effect of coapplication of the potentiating neurosteroid allopregnanolone (3α5αP) and EPA on currents elicited by GABA. The cell was exposed to 0.5 μM GABA, GABA+30 μM EPA, GABA+100 nM allopregnanolone or GABA+EPA+allopregnanolone. The presence of EPA did not reduce the potentiation by allopregnanolone, suggesting that EPA is not a high-affinity, low-efficacy modulator acting through the steroid-binding site. The peak amplitudes were 77 pA (GABA alone), 186 pA (GABA+EPA), 551 pA (GABA+allopregnanolone) and 1506 pA (GABA+allopregnanolone+EPA). The averaged values from all experiments are given in the text. (c) The effect of EPA on receptors directly activated by allopregnanolone. The cell was exposed to 10 μM allopregnanolone (3α5αP), or allopregnanolone+30 μM EPA. The presence of EPA potentiated the current response, suggesting that the sites for allopregnanolone and EPA are non-overlapping. The peak amplitudes were 183 pA (allopregnanolone) and 324 pA (allopregnanolone+EPA). The averaged values from all experiments are given in the text. Exposure to 30 μM EPA alone did not elicit a discernible current (data not shown).