Methylazoxymethanol treatment of fetal rats results in abnormally dense noradrenergic innervation of neocortex.
A single injection of methylazoxymethanol in pregnant rats at 15 days of gestation results in severe cortical atrophy in the offspring. In the adult offspring, the neurochemical markers for the cortical gamma-aminobutyric acid-containing neurons are severely reduced, whereas the noradrenergic markers are minimally altered. Immunohistofluorescence microscopy demonstrates a marked increase in the density of noradrenergic axons which have an abnormal pattern of distribution in the atrophic cortex. The results suggest that the central noradrenergic neurons determine the number of axons to be formed early in brain development, but local factors in the terminal field regulate the ultimate distribution of the noradrenergic axons.
D000320:Adrenergic Fibers / Q000166:cytology / Q000196:embryology*; D000818:Animals; D001391:Azo Compounds / Q000494:pharmacology*; D001921:Brain / Q000166:cytology / Q000196:embryology*; D002454:Cell Differentiation / Q000187:drug effects; D002540:Cerebral Cortex / Q000196:embryology / Q000201:enzymology; D005968:Glutamate Decarboxylase / Q000378:metabolism; D008746:Methylazoxymethanol Acetate / Q000494:pharmacology*; D009434:Neural Pathways / Q000196:embryology; D009638:Norepinephrine / Q000378:metabolism; D051381:Rats; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D001391:Azo Compounds; D005680:gamma-Aminobutyric Acid; D008746:Methylazoxymethanol Acetate; D014446:Tyrosine 3-Monooxygenase; D005968:Glutamate Decarboxylase; D009638:Norepinephrine