Robertson_1990_Int.J.Dev.Neurosci_8_223

Previous studies have demonstrated that acetylcholinesterase (AChE) activity is expressed transiently by thalamocortical neurons of primary sensory systems in developing rat pups. In the present study, prenatal treatment with methylazoxymethanol acetate (MAM) on embryonic day 15, 16, or 17 resulted in rat pups with cerebral cortices markedly reduced in thickness and areal extent. Histochemical studies demonstrated that AChE staining occurs in fiber-like plexuses in primary visual, auditory, and somatosensory regions of developing cerebral cortex of MAM-treated animals, just as in normal developing rats, but that the transient patterns of AChE are found more superficially than normal and they occur in an abnormal patchy distribution. Neuronal somata in thalamic lateral geniculate, medial geniculate and ventral basal nuclei of MAM-treated animals show transient AChE staining indistinguishable from that seen in normal animals. These data indicate: (1) AChE is expressed transiently by thalamocortical neurons in MAM-treated animals, (2) intensity of the transiently expressed AChE is not affected by MAM-induced loss of cortical neurons, and (3) the abnormal AChE patterns in cortex likely reflect the abnormal distributions of thalamocortical terminal fields that are characteristic of MAM-treated animals.