[smart (OP)]

The Wikipedia page on phospholipase C (PLC) says that activation (phosphorylation) of PLC is coupled to GPCR receptors. However, the cannabinoid type 1 receptor (CB1) is also a GPCR, but no mention is made about intracellular CB1 activation of phospholipase C.

See: https://en.wikipedia.org/wiki/Phospholipase_C#Regulation

[smart (OP)]

Phosphorylation-induced activation of PLC by cannabinoid receptors has huge implications
for its physiological role in the metabolism of arachidonic acid:

Additionally, phospholipase C plays an important role in the inflammation pathway. The binding of agonists such as thrombin, epinephrine, or collagen, to platelet surface receptors can trigger the activation of phospholipase C to catalyze the release of arachidonic acid from two major membrane phospholipids, phosphatidylinositol and phosphatidylcholine. Arachadonic acid can then go on into the cyclooxygenase pathway (producing prostoglandins (PGE1, PGE2, PGF2), prostacyclins (PGI2), or thromboxanes (TXA2)), and the lipoxygenase pathway (producing leukotrienes (LTB4, LTC4, LTD4, LTE4)).[22]

https://en.wikipedia.org/wiki/Phospholipase_C#Biological_function

[smart (OP)]

I updated the PLC wikipedia page to indicate that cannabinoid receptors are functional PLC ligands activated via GPCR mecanism.