CNR1 and neuroblastoma: In thesecells, 2–11,12-EG induced activation of downstream p44/p42ERKs (extracellular signal-regulated kinases), which could be inhibitedby CB1 or CB2 antagonism and pertussis toxin, but not by adenylatecyclase, protein kinase A, or phospholipase C inhibitors, which suggestedthe involvement of receptors coupled to Gi/o proteins.2-EG also activated ERK signaling in N182G2 neuroblastoma cells, whichexpress endogenous CB1 but not CB2 receptors.