Postsynaptic location of acrylamide-induced modulation of striatal 3H-spiroperidol binding.
The striata of rats were unilaterally lesioned with kainic acid. After two weeks, rats were exposed to 10 doses of acrylamide (20 mg/kg body weight/dose) over two weeks. Binding of 3H-spiroperidol to membranes prepared from unoperated striata, was elevated in acrylamide-exposed rats relative to undosed controls. This differential was not apparent when binding was compared in membranes from kainate-treated striata of acrylamide-treated and untreated rats. A parallel acrylamide treatment of unoperated rats had no significant effect on striatal levels of dihydroxyphenylacetic acid and homovanillic acid suggesting that this neurotoxicant failed to affect the presynaptic events of the dopamine system. Thus, the alterations of the striatal dopamine receptor caused by acrylamide, that have been previously reported, appear to be confined to postsynaptic sites.
D000178:Acrylamides / Q000009:adverse effects*; D000818:Animals; D002090:Butyrophenones / Q000378:metabolism*; D003342:Corpus Striatum / Q000187:drug effects* / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism; D008297:Male; D051381:Rats; D011916:Rats, Inbred F344; D011954:Receptors, Dopamine / Q000187:drug effects*; D013134:Spiperone / Q000378:metabolism*; D014316:Tritium
D000178:Acrylamides; D002090:Butyrophenones; D011954:Receptors, Dopamine; D014316:Tritium; D013134:Spiperone; D004298:Dopamine