Cannabinoids activate p38 mitogen-activated protein kinases through CB1 receptors in hippocampus.

摘要: Cannabinoid receptors (CB1-R) are the target of a novel class neuromodulators, endocannabinoids. Yet, their signalling mechanisms in adult brain poorly understood. We report that, rat and mouse hippocampal slices, anandamide 2-arachidonoylglycerol, synthetic cannabinoids, delta(9)-tetrahydrocannabinol activated p38 mitogen-activated protein kinases (MAPK), but not c-Jun N-terminal kinase (JNK). In contrast, lysophosphatidic acid (LPA), lipid messenger acting on different receptors, increased both p38-MAPK JNK phosphorylation. The effects cannabinoids were mediated through activation CB1-R because they blocked presence SR 141716 A absent knockout mice, two conditions that did alter LPA. by was insensitive to inhibitors SRC: These results provide new insights into cellular which exert hippocampus.