Antagonism by abecarnil of enhanced acetylcholine release in the rat brain during anticipation but not consumption of food

Changes in the extracellular concentration of acetylcholine (ACh) were evaluated in the prefrontal cortex and hippocampus of freely moving rats habituated for 35 days to consume their daily meal during a fixed 2-h period. During the 40 min immediately before presentation, ACh output increased by 49 and 55% in the prefrontal cortex and hippocampus, respectively. ACh release increased further during the first 40 min of consumption phase in the prefrontal cortex (+220%) and hippocampus (175%). Administration of abecarnil (0.1 mg/kg, IF) 40 min before food presentation prevented the increase in ACh output in both brain regions during the anticipatory phase. In contrast, although abecarnil reduced the ACh content achieved during the consummatory phase, it did not prevent the increase in ACh release in the prefrontal cortex or hippocampus induced by food intake. Finally, the binding of [S-35]TPBS to cerebral cortex, hippocampus: or septum of rats killed 20 min before food presentation was significantly higher than the values for animals killed 2 h after food presentation. These results suggest that during ingestive behavior ACh release is regulated by at least two independent mechanisms: one, associated with the anticipatory phase, that is sensitive to the activation of GABA(A) receptors, and a second, associated with the consummatory phase, that is insensitive to abecarnil. (C) 1998 Elsevier Science Inc.