Neurotransmitter chemistry of lissencephalic cortex induced in ferrets by fetal treatment with methylazoxymethanol acetate.
Treatment of pregnant ferrets with 15 mg/kg of methylazoxymethanol acetate (MAM) at 33 days of fetal gestation results in offspring with cortical hypoplasia and lissencephally. Neurochemical analysis of 5 areas of cortex from 8-week-old offspring of MAM- or vehicle-treated jills indicated an overall enrichment in markers for catecholaminergic (tyrosine hydroxylase, norepinephrine) and cholinergic (choline acetyltransferase, acetylcholine) terminals but minimal change in the concentration of GABAergic markers (glutamate decarboxylase, gamma-aminobutyric acid); however, there did not appear to be a direct, inverse relationship between the concentration of catecholaminergic and cholinergic markers and the degree of hypoplasia in cortical subareas unlike what has been found previously in the rat.
D000818:Animals; D001391:Azo Compounds / Q000494:pharmacology*; D002335:Carnivora / Q000196:embryology*; D002540:Cerebral Cortex / Q000187:drug effects / Q000196:embryology / Q000502:physiology*; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D005260:Female; D005289:Ferrets / Q000196:embryology*; D005333:Fetus; D005968:Glutamate Decarboxylase / Q000378:metabolism; D008746:Methylazoxymethanol Acetate / Q000494:pharmacology*; D009928:Organ Specificity; D011247:Pregnancy; D009435:Synaptic Transmission / Q000187:drug effects*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D001391:Azo Compounds; D008746:Methylazoxymethanol Acetate; D014446:Tyrosine 3-Monooxygenase; D002795:Choline O-Acetyltransferase; D005968:Glutamate Decarboxylase