ABSTRACT
It has been shown that the endocannabinoids inhibit luteinizing hormone (LH) and prolactin (PRL) secretion. When the effects of the two well-known endocannabinoids arachidonoylethanolamide (AEA, anandamide) and 2-arachidonoyl-glycerol (2AG) have been compared it became evident that AEA caused inhibition was higher than that one of 2AG. AEA also diminished the two investigated hormonal levels in CB1 receptor inactivated mice. AEA, being an endogenous ligand of vanilloid type 1 (TPRV1) receptor, while activating TPRV1 receptor has an effect on both LH and PRL levels decrease because these later were abolished when capsazepin, antagonist of TPRV1 receptor was previously administered to the CB1 KO animals. We postulate that the difference between the effects of AEA and 2AG on the serum levels of LH and PRL is due to the difference in receptor activation of these two compounds, namely AEA can activate both CB1 and TRPV1 receptor but 2AG acts only on CB1 receptor.
