Fig. 5.

Dendritic ER_αdrives 2-AG signaling in females. a) Raw traces from single experiments (top) and time course of averaged experiments (bottom left) show that increasing tonic AEA via inhibition of FAAH (URB, 1 μM) does not occlude eCB signaling via ER_α (PPT, 200 nM). A summary of the URB_PPT occlusion experiments is shown bottom, right. These suggest that ER_α stimulation does not drive AEA production. Each * indicates significant differences from baseline responses; #s indicate significant differences between URB (last 5 min and URB + PPT (last 5 min) (p ≤ 0.05), one-way rmANOVAs. b) Raw traces from single experiments (top) and time course of averaged experiments (bottom left) show that increasing tonic 2-AG via inhibition of MAGL (JZL, 100 nM) does occlude eCB signaling via ER_α (PPT, 200 nM). A summary of the JZL_PPT occlusion experiments is shown right; indicating that ER_α stimulation does drive 2-AG production. Each * indicates significant differences from baseline responses (p ≤ 0.05), one-way rmANOVAs. c) Raw traces from single experiments (top) and time course of averaged experiments (bottom left) show that decreasing tonic 2-AG via inhibition of DAGL (DO34, 1 μM) not only blocks eCB signaling via ER_α (PPT, 200 nM), but leads to a decrease in female fEPSPs. A summary of the DO34_PPT occlusion experiments is shown right. n = number of slices per experiment. Each * indicates significant differences from baseline responses; #s indicate significant differences between DO34 (last 5 min and DO34 (last 5 min) (p ≤ 0.05), one-way rmANOVAs.