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 r ats habituated for 35 days to consume their daily meal during a fixed 2-h period. During the 40 min immediately before presentation, ACh out put 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 (1 75%). Administration of abecarnil (0.1 mg/kg, IF) 40 min before food p resentation prevented the increase in ACh output in both brain regions during the anticipatory phase. In contrast, although abecarnil reduce d the ACh content achieved during the consummatory phase, it did not p revent the increase in ACh release in the prefrontal cortex or hippoca mpus induced by food intake. Finally, the binding of [S-35]TPBS to cer ebral cortex, hippocampus: or septum of rats killed 20 min before food presentation was significantly higher than the values for animals kil led 2 h after food presentation. These results suggest that during ing estive behavior ACh release is regulated by at least two independent m echanisms: one, associated with the anticipatory phase, that is sensit ive to the activation of GABA(A) receptors, and a second, associated w ith the consummatory phase, that is insensitive to abecarnil. (C) 1998 Elsevier Science Inc.