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. Author manuscript; available in PMC: 2014 Jan 1.
Published in final edited form as: Neuroendocrinology. 2012 Aug 28;97(2):160–175. doi: 10.1159/000338669

Fig. 6.

Fig. 6

17α-estradiol does not affect the cannabinoid-induced presynaptic inhibition of glutamatergic synaptic input onto POMC neurons. A, Spontaneous mEPSCs in a cell perfused with 100 nM 17α-estradiol at baseline (left) and following exposure to 1 μM WIN 55,212-2 (right). B, The cumulative probability plot illustrating the interval between contiguous mEPSCs that substantiates the inability of 17α-estradiol to attenuate the inhibitory effect of WIN 55,212-2 on mEPSC frequency. *, Distribution of the mEPSC interval in the presence of WIN 55,212-2 that is significantly different (Kolmogorov-Smirnov test, p<.05) than that observed under basal conditions. C, The composite bar graph illustrating the stereospecificity of the E2-induced diminution of the decrease in mEPSC frequency caused by WIN 55,212-2. Bars represent means and vertical lines 1 SEM of the cannabinoid receptor agonist-induced decrease in mEPSC frequency normalized to baseline control conditions. *, Values measured in E2-treated slices that are significantly different (Kruskal-Wallis test/median-notched Box-and-Whisker plot; p<.05; n=5–8) than those measured in the other treatment conditions.