Fetally-induced noradrenergic hyperinnervation of cerebral cortex results in persistent down-regulation of beta-receptors.
Methylazoxymethanol acetate (MAM)-induced cortical hypoplasia resulted in a 2-fold increase in the concentration of norepinephrine and its metabolite, 3-methoxyl-4-hydroxyphenylglycol sulfate, and a 26% decrease in the Bmax for the beta-receptor ligand, [3H]dihydroalprenolol (DHA) in the rat cortex. Chronic treatment with desmethylimipramine did not further decrease DHA-labeled sites although prior lesion of the noradrenergic terminals with 6-hydroxydopamine markedly increased the number in the MAM-lesioned cortex.
D000818:Animals; D001391:Azo Compounds / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000187:drug effects*; D003891:Desipramine / Q000494:pharmacology; D004082:Dihydroalprenolol / Q000378:metabolism; D005260:Female; D006892:Hydroxydopamines / Q000494:pharmacology; D007700:Kinetics; D008431:Maternal-Fetal Exchange / Q000187:drug effects; D008746:Methylazoxymethanol Acetate / Q000494:pharmacology*; D009474:Neurons / Q000187:drug effects; D009638:Norepinephrine / Q000378:metabolism*; D016627:Oxidopamine; D011247:Pregnancy; D051381:Rats; D011919:Rats, Inbred Strains; D011941:Receptors, Adrenergic / Q000187:drug effects*; D011943:Receptors, Adrenergic, beta / Q000187:drug effects*
D001391:Azo Compounds; D006892:Hydroxydopamines; D011941:Receptors, Adrenergic; D011943:Receptors, Adrenergic, beta; D008746:Methylazoxymethanol Acetate; D004082:Dihydroalprenolol; D016627:Oxidopamine; D003891:Desipramine; D009638:Norepinephrine