PAK1 regulates inhibitory synaptic transmission in mice through a cyclooxygenase-2 dependent restriction in tonic, but not phasic, secretion of endocannabinoids.

The molecular mechanisms beyond the bidirectionality (tTLP and tLTD) of endocanabinoid spike-timing dependent synaptic plasticity have been identified.

Endocannabinoids modulate ventral hippocampal inputs to the infralimbic prefrontal cortex by dampening feed-forward inhibition mediated by cholecystokinin-expressing (CCK+) interneurons onto layer 5 intratelencephalic (IT) cells.

Non-synaptic extracellular vesicles may be involved in the release of endogenous cannabinoids in the central nervous system thereby representing a novel mechanism to mediate their effects on synaptic transmission.

Oxytocin, a peptide linked to the processing of socially meaningful stimuli, modulates excitatory synaptic transmission in dopaminergic neurons of ventral tegmental area via retrograde endocannabinoid signaling, acting as a pathway-specific temporal filter for synaptic inputs.

A mouse model of Williams–Beuren syndrome allowed us to assess the endocannabinoid system and the impact of targeting the monoacyl glycerol lipase in modulating key phenotypes such as cognitive and hypersocial phenotype as well as the cardiac phenotype.

The hepatic endocannabinoid/CB₁R system controls the soluble leptin receptor’s expression and/or subsequent release by Trib3-induced regulation of C/EBP homologous protein levels in hepatocytes to affect leptin signaling in the liver.

Cell-specific pathways regulate lipid transmitters and neuroinflammation in the brain.

Endocannabinoid activation of the CB1 receptor on retinal ganglion cells in the eye results in enhanced excitability and responsiveness to visual stimulation through a novel mechanism involving intracellular chloride regulation.

Sleep deprivation enhances energy-dense food choices and encoding of olfactory information in the human brain.