Effects of foetal treatment with methylazoxymethanol on noradrenergic synapses in rat cerebral cortex

Abstract

Methylazoxymethanol (MAM)-induced cerebral hypoplasia resulted in a significant increase in densities of norepinephrine uptake sites in cerebral cortex, suggesting that norepinephrinergic axon terminals were compressed in the smaller brain volumes. The density of beta-adrenergic receptors in MAM-lesioned cerebral cortex was decreased probably due to down-regulation, while there were no changes in the proportions and affinities of agonist high-affinity sites and agonist low-affinity sites in the desensitized beta-receptors.