Fetal methylazoxymethanol acetate-induced lesions cause reductions in dopamine receptor-mediated catalepsy and stereotypy.
Telencephalic hypoplasia induced by methylazoxymethanol acetate (MAM) resulted in increased activity of tyrosine hydroxylase in the striatum, indicative of a relative increase in the density of dopaminergic terminals in the remaining tissue. Administration of the dopamine receptor stimulant, apomorphine, or the receptor blocker, haloperidol, produced less stereotypy and catalepsy, respectively, in rats lesioned with methylazoxymethanol, compared to controls. These behavioral changes probably resulted from the loss of striatal perikarya and consequent decrease in nigrostriatal dopaminergic target sites caused by methylazoxymethanol.
D000818:Animals; D001391:Azo Compounds / Q000633:toxicity*; D001921:Brain / Q000201:enzymology; D001923:Brain Chemistry / Q000187:drug effects; D002375:Catalepsy / Q000139:chemically induced*; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D003864:Depression, Chemical; D005260:Female; D005333:Fetus / Q000187:drug effects*; D005968:Glutamate Decarboxylase / Q000378:metabolism; D006220:Haloperidol / Q000494:pharmacology; D007700:Kinetics; D008746:Methylazoxymethanol Acetate / Q000633:toxicity*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000187:drug effects*; D013239:Stereotyped Behavior / Q000187:drug effects*
D001391:Azo Compounds; D011954:Receptors, Dopamine; D008746:Methylazoxymethanol Acetate; D002795:Choline O-Acetyltransferase; D005968:Glutamate Decarboxylase; D006220:Haloperidol