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3. Umbruch 4.4..2005 - Online Pot

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Endocannabinoids and regulation of fertility 71<br />

Figure 2. Interactions between blastocyst and uterine epithelium. At the site of implantation blastocysts<br />

release a lipid compound able to activate fatty acid amide hydrolase (FAAH) in uterine epithelial<br />

cells, termed the FAAH activator. This leads to the cleavage of anandamide (AEA), thus reducing<br />

its uterine levels and noxious effects towards the implanting blastocyst (see also Fig. 1). AEA-synthesizing<br />

phospholipase D (PLD), AEA membrane transporter (AMT) and AEA-binding type 1<br />

cannabinoid receptors (CB 1Rs) of uterine epithelial cells are not modulated by the FAAH activator.<br />

production of the activator by an unhealthy embryo might contribute to<br />

implantation failure. Alternatively, a non-receptive, unhealthy uterus might be<br />

unable to respond properly to a normal activator, leading to blastocyst death.<br />

Though the molecular details of the embryo–uterine cross-talks remain to be<br />

elucidated, present evidence strongly suggests that FAAH regulates these<br />

cross-talks by controlling the endogenous tone of AEA.

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