Filomena Fezza

TL;DR: It is shown that following temporary food restriction, CB1 receptor knockout mice eat less than their wild-type littermates, and the CB1 antagonist SR141716A reduces food intake in wild- type but not knockout mice, which indicates that endocannabinoids in the hypothalamus may tonically activate CB1 receptors to maintain food intake and form part of the neural circuitry regulated by leptin.

TL;DR: The hypothesis, based on previous structure-activity relationship studies and the availability of biosynthetic precursors, that N-arachidonoyl-dopamine (NADA) is an endogenous “capsaicin-like” substance in mammalian nervous tissues is examined and found that NADA occurs in nervous tissues.

TL;DR: These findings provide the first direct evidence of altered brain levels of endocannabinoids, and of 2‐AG in particular, during fasting and feeding, and supports a role for endoc cannabinoidoids in the control of appetitive motivation.

TL;DR: These studies provide definitive evidence for the tonic control of spasticity by the endocannabinoid system and open new horizons to therapy of multiple sclerosis, and other neuromuscular diseases, based on agents modulating endoc cannabinoidoid levels and action, which exhibit little psychotropic activity.

TL;DR: It is found that stimulation of metabotropic glutamate 5 receptors by 3,5-dihydroxyphenylglycine (DHPG) depressed inhibitory transmission in the striatum through selective involvement of 2-AG metabolism and stimulation of presynaptic CB1 receptors.