UC Irvine

Acrylamide was administered orally to 6 week old male rats in ten doses, spread over a two week period. At the two lower doses (5 and 10 mg/kg, total dose 50 and 100 mg/kg) effects on neurotransmitter receptor sites appeared confined to the striatum where both the dopamine and muscarinic acetylcholine receptors exhibited enhanced binding twenty four hours after the last acrylamide dose. Other receptor sites within the frontal cortex, cerebellum, and medulla were not significantly altered. At the highest dose (20 mg/kg, given ten times), increases were also found for frontal cortical serotonin, medullary glycine, and cerebellar GABA receptor sites. The only unaffected receptor found was the cortical site for benzodiazepene. One week after the final acrylamide dose, the intensity of binding of all ligands studied was not significantly different in treated and control groups. Thus, effects appeared reversible. Since striatal membrane protein concentration was reduced by treatment of rats with acrylamide, the observed increased in activity of muscarinic receptors could be best accounted for in terms of loss of striatal non-receptor protein rather than increased binding. However, the magnitude of increased striatal 3H-spiroperidol binding in treated animals suggested an increase in overall binding capacity. An effect on dopamine neurons was also suggested by a decreased responsiveness to apomorphine in rats treated with acrylamide at 10 mg/kg for 10 successive days; however, the effect had dissipated by 8 days after the final injection of acrylamide.