Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
4326690 | Brain Research | 2010 | 8 Pages |
Studies have demonstrated defects of DA and 5 HT neurotransmission in dietary fat induced obese animals. In the present study, we used a perfusion system to assay the release of DA and 5 HT from striatal slices preloaded with [3H]-DA or [3H]-5 HT. The release of both DA and 5 HT from striatal slices of rats fed a high fat diet for 10 days, but not 3 days, was reduced when compared to striatal slices taken from rats fed a low fat diet. Enterostatin, an endogenous pentapeptide inhibits dietary fat intake when administered peripherally and centrally in animals. The central mechanism for the action of enterostatin is not yet determined even though several mechanisms have been suggested. We have shown that enterostatin enhanced [3H]-DA release, but not [3H]-5HT release from striatal slices of rats that had been adapted to high fat diet for 10 days. The enterostatin-induced increase in [3H]-DA release was blocked by nomifensine. Enterostatin did not alter [3H]-DA or [3H]-5HT release from striatal slices of rats adapted to high fat or low fat diet feeding for 3 days. These findings suggest that enterostatin may inhibit dietary fat intake by blocking dopamine reuptake transport to increase central striatal DA release from rats that have acquired diminished dopamine signal after an adaptive period of fat consumption.