Abstract
In the D3 receptor, buspirone showed a pose similar to that of SB27711A, confirming the experimental data about its antagonist activity at D3 receptor. Docking at 5-HT1A showed no favorable binding of SB277011A and alternative poses for buspirone. Conclusions: RACK1/BDNF/D3R pathway seems to operate as a reinforcing mechanism in voluntary ethanol intake. The pharmacological effects of D3R antagonism, decreasing alcohol intake in C57BL/6J WT mice, indicate the D3 receptor as a promising therapeutic target for alcohol weaning. Moreover the optimized structure models of drug-targets seems useful in understanding at atomistic and molecular level the pharmacological effects of the drugs investigated and may represent important tools in drug discovery of therapeutic agents for addiction.
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