These data indicate that membrane GPER mediates the E2/E-Biotin facilitation of lordosis by inducing OFQ/N neurotransmission, which inhibits β-END neurotransmission to reduce MPN MOP activation.
In addition, GPER1 activation contributes to behaviors that denote anxiety and to social behaviors such as social memory and lordosis behavior in mice.
The results suggest that GnRH release activates both estrogen and progestin receptors and that this activation is important in the chain of events leading to the display of lordosis behavior in response to activation of GPER-1 in estrogen-primed rats.
G1 did not mimic E(2) negative-feedback inhibition of LH secretion, and GPR30 RNAi did not interfere with E(2) suppression of LH or facilitation of lordosis behaviour.