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.