Fig. 2
From: The grass isn’t always greener: The effects of cannabis on embryological development
CB1 cannabinoid receptor signaling and regulation of neural stem/progenitor cell proliferation. CB1 receptors are coupled to Gi proteins, thereby mediating the inhibition of adenylyl cyclase (AC) and protein kinase A (PKA). CB1 receptor coupling to Gi signalling is also associated with activation of the extracellular signal-regulated kinase (ERK) pathway via different mechanisms. Direct activation of the PI3K/Akt and ERK pathways by CB1 receptors may converge, thus synergizing with their activation by other receptors such as growth factor receptors with tyrosine kinase activity (RTK). CB1 receptor-induced activation of RTKs can occur by promoting the processing of membrane-bound growth factor inactive precursors to yield active growth factors, or by activating intracellular Src family protein kinases. In some circumstances, CB1 activity can antagonize RTK-mediated ERK signaling. Activation of the CB1 receptor ultimately controls different transcriptional regulators, including CREB, STAT-3, PAX-6 and β-catenin. The CB1 receptor may also regulate mammalian target of rapamycin complex 1 (mTORC1) in NPs as it occurs in differentiated neurons. Permission to use figure was obtained from [44] and Creative Commons (https://creativecommons.org/licenses/by/4.0/)