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. 2001 Jan 30;98(3):793–795. doi: 10.1073/pnas.98.3.793

Figure 1.

Figure 1

Two models that could account for the molecular mechanism underlying the cross talk between Δ9-tetrahydrocannabinol (THC), progesterone, and dopamine. (A) THC, progesterone, and dopamine act through CB1, progestin (PR), and dopamine D1B receptors, respectively. If the same target cell expresses these three receptors, a cross talk that involves mitogen-activated protein kinase (MAPK) could take place. (B) THC acts through CB1 receptors expressed on dopaminergic terminals, increasing the release of dopamine. Dopamine would then activate D1B receptors, which in turn stimulate the cAMP–protein kinase A, a pathway leading to the phosphorylation of dopamine and cAMP regulated phosphoprotein 32 (DARPP-32) (29).