Abstract
Abstract Lesions of the nucleus basalis magnocellularis (NBM) have been employed to produce biochemical deficits of the central cholinergic system. In the present study microinjection of aziridinium ion analogs of hemicholinium (4 nmol) into the NBM of young adult rats was found to significantly decrease choline acetyltransferase (ChAT) activity, but not glutamic acid decarboxylase (GAD) activity in the ipsilateral cerebral cortex and NBM. No changes were observed in either the hippocampus or striatum. The decrease in cortical ChAT activity was observed at four, seven and thirty days post-lesion. Immunocytochemical analysis of the NBM cholinergic neurons revealed somatic shrinkage and loss of cellular processes following the treatment with neurotoxin, without evidence of non-specific neural damage. Cortical administration of the monosialoganglioside GM1 (10 mg/gel) prevented the observed decrease in ChAT in both the cortex and NBM. The biochemical and immunocytochemical results are in agreement with both the reported cholinotoxic effects of hemicholinium aziridinium analogs and the reported protective effects of GM1 following brain injury in different animal models.
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