| pubmed-article:6141297 | pubmed:abstractText | The effects of lesions induced by fetal treatment with methylazoxymethanol acetate (MAM) on the developmental synaptic chemistry of the frontal cortex of rats were examined. Treatment at 14 days' gestation (DG) resulted in a 50% decrease in frontal cortical mass whereas treatment at 15 DG caused a 40% decrement. No difference in concentration between MAM and control rats was observed in the postnatal development of the GABA-ergic markers, glutamate decarboxylase, and GABA. In contrast, the concentrations of the presynaptic markers for the dopaminergic, noradrenergic, and serotonergic terminals were generally elevated in the MAM lesioned frontal cortex throughout postnatal development. The effects of MAM lesion on cholinergic markers were mixed, with minimal alterations in concentration during the first 2 postnatal weeks followed by an increasing disparity thereafter. The results of this study provide additional evidence in support of the differential impact of the cortical hypoplasia on intrinsic neurons as contrasted to aminergic afferents. | lld:pubmed |
