ABSTRACT
When released into the interneural cleft, they act retro-
gradely on the presynaptic cannabinoid receptor (CB-1), a
seven-membrane-spanning G-coupled receptor. Activation
of this receptor by endogenous or exogenous cannabinoid
inhibits the release of g-aminobutyric acid and thus removes an inhibitory influence of “satiety” signals, allow-
ing the positive feedback for palatable food to drive eating.
Blockade of the CB-1 receptors turns this system off and
induces satiety. The brain content of the endogenous 2-
arachidonoyl-glycerol is reduced in fed animals where
satiation has occurred and is high in “hungry” animals
who want to eat. As anticipated, these endogenous canna-
binoids will stimulate food intake.
