Pathogenesis of methylazoxymethanol-induced lesions in the postnatal mouse cerebellum.
Previous studies have shown that methylazoxymethanol acetate (MAM) and methylazoxymethanol glucoside (cycasin) cause destruction of differentiation cells in the postnatal mouse cerebellum. The major features of the resulting architectural disarray were Purkinje cell misalignment and granule cell deletion along with cerebellar dysfunction. Although it was clear from a number of studies that destruction of differentiation cells in the immediate postnatal period was the primary lesion, several important facets of the pathellular response to the injury was incompletely described. The relationship of the cellular response to the subsequent pathological alterations was not completely evaluated. Also, the presence of unattached Purkinje cell dendritic spine postsynpatic sites suggested that their development had occurred without presynaptic parallel fiber terminal differentiation. The possibility of early synaptogenesis and degeneration was not, however, completely ruled out.
D000818:Animals; D001253:Astrocytes / Q000187:drug effects; D001391:Azo Compounds / Q000494:pharmacology*; D002454:Cell Differentiation / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D002531:Cerebellum / Q000166:cytology / Q000187:drug effects* / Q000473:pathology; D008746:Methylazoxymethanol Acetate / Q000494:pharmacology*; D051379:Mice; D008928:Mitochondria / Q000187:drug effects; D009474:Neurons / Q000187:drug effects; D011689:Purkinje Cells / Q000187:drug effects; D013569:Synapses / Q000187:drug effects; D013572:Synaptic Vesicles / Q000187:drug effects; D013997:Time Factors
D001391:Azo Compounds; D008746:Methylazoxymethanol Acetate