We have previously shown that neonatal lesions of the basal forebrain cholinergic afferents result in transient cholinergic depletion concomitant with abnormal morphogenesis of cerebral cortex in Balb/CByJ mice (Höh mann et al., 1988). Here, we have utilized the rapid Golgi method to further characterize these previously observed abnormalities. We compared layer V pyramidal neurons in somatomotor cortex ipsi-and contralateral to the lesion at postnatal days (PND) 7 and 14. Quantitative evaluations showed a significant reduction in all aspects of the dendntic tree as well as in cell body size in ipsilateral cortex at PND 7. Differences between ipsiand contralateral pyramidal cells had attenuated by PND 14, but significant somatic size differences persisted, as did changes in the apical branching pattern. Qualitative differences between ipsilateral and contralateral hemispheres included the relatively more immature ap pearance of ipsilateral neurons at both ages, in addition to unusual dendritic morphology, particularly at PND 14. A close correlation was apparent between the magnihide of cholinergic depletion in cortex (larger at PND 7 than at PND 14) and the severity of abnormalities in pyramidal cell morphogenesis. We conclude that a normal cholinergic innervation to neocortex is instrumental in the timely differentiation of cortical neurons, because neonatal nBM lesions disrupted the time schedule of differentiation, but did not preclude the pyramidal neu rons from further differentiation at a later time.

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