3. Umbruch 4.4..2005 - Online Pot

70 M. Maccarrone
Figure 1. Local effects of anandamide on implantation and uterine changes. Binding of anandamide
(AEA) to type 1 cannabinoid receptors (CB 1Rs) on the blastocyst leads to cell death, whereas its binding
to CB 1 receptors on the uterine epithelium inhibits gap junctions and is instrumental in modifying
the uterus during gestation. The AEA membrane transporter (AMT) and the fatty acid amide
hydrolase (FAAH) present in the uterine epithelial cells cleave AEA into ethanolamine (EtNH 2) and
arachidonic acid (AA), thus protecting the blastocyst against the noxious effects of AEA.
Progesterone (P) and estrogen (E 2) down-regulate uterine FAAH. Also the blastocyst has active AMT
and FAAH (omitted for the sake of clarity), which dispose of AEA and facilitate implantation.
FAAH activator is released by the implanting blastocysts further corroborates
the hypothesis that these cells need to protect themselves against the noxious
effects of uterine endocannabinoids. A lipid able to cross the cell membranes
and to rapidly and specifically activate FAAH in uterine epithelial cells is suitable
to confer this protection, as schematically shown in Figure 2. A defective