data suggest that the various PKC isoforms may possibly differentially contribute to opioid regulation of glucose transport as a function of the opioid receptor subtype, rather than the cell type involved. d Opioid receptor agonists have demonstrated an ability to exert neuroprotective and cardio-protective results under hypoxic and ischaemic insults. As GLUT1 is commonly expressed, it is very important to investigate whether an Aurora B inhibitor increased GLUT1 activity might give rise to the beneficial effects of d opioid receptor agonists in problems of limited energy supply, and whether this property could be used to develop new pharmacological techniques for improving glucose utilization in conditions characterized by improved glucose homeostasis. Endocannabinoids have both anti-inflammatory and neuroprotective properties against harmful stimuli. We previously demonstrated that the endocannabinoid 2 arachidonoylglycerol protects hippocampal neurons by limiting the inflammatory response using a CB1 receptor dependent MAPK/NF kB signalling pathway. The purpose Lymphatic system of today’s study was to find out whether PPARg, a significant nuclear receptor, mediates 2 AG induced inhibition of NF kB phosphorylation and COX 2 expression, and COX 2 increased tiny spontaneous excitatory postsynaptic currents. FRESH APPROACH By using a whole cell patch clamp electrophysiological recording technique and immunoblot analysis, we determined mEPSCs, expression of COX 2 and PPARg, and phosphorylation of NF kB in mouse hippocampal neurons in culture. CRUCIAL RESULTS endogenous and Exogenous 2 AG produced suppressions of NF kB p65 phosphorylation, COX 2 expression and excitatory synaptic transmission in response to pro-inflammatory interleukin 1b and LPS were inhibited by GW9662, a selective PPARg antagonist, in hippocampal neurons in culture. PPARg agonists 15 deoxy D12,14 prostaglandin J2 and rosiglitazone mimicked the effects of 2 AG on NF kB p65 phosphorylation, COX 2 expression and mEPSCs, and these effects were eliminated by antagonism of PPARg. Moreover, exogenous application of 2 AG or level of endogenous 2 AG by inhibiting its hydrolysis with URB602 order Lonafarnib or JZL184, selective inhibitors of monoacylglycerol lipase, stopped the IL 1band LPS induced reduction of PPARg appearance. The 2 AG restoration of the reduced PPARg expression was blocked or attenuated by pharmacological or genetic inhibition of the CB1 receptor. Our results suggest that CB1 receptor dependent PPARg expression is an essential and novel signalling pathway in endocannabinoid 2 AG produced resolution of neuroinflammation in reaction to pro-inflammatory insults. RELATED ARTICLES This short article is a part of a themed concern on Cannabinoids in Medicine and Biology.