A single oral dose of acrylamide (25 or 50 mg/kg) increased the level of striatal 3H-spiroperidol binding in six week old male rats. This enhanced dopamine receptor activity was specific since treatment caused no significant changes in glycine, serotonin, and muscarinic cholinergic binding. At the highest acrylamide dose tested (100 mg/kg), elevations of the medullary glycine and frontal cortical serotonin receptors were also found. Pretreatment of animals with a blocker of hepatic mixed function oxidase (SKF 525a) or a thiol blocker (methylmercuric chloride) prevented the acrylamide-induced elevation of striatal spiroperidol binding, indicating that the causative agent was a secondary metabolite of acrylamide. Apomorphine-induced motility was significantly attenuated by 24 hr predosing with acrylamide, suggesting a change in the sensitivity of the dopamine receptor. The behavioral relevance of observed biochemical changes was thus shown by the altered response of treated animals to apomorphine
