CHOLINE-ACETYLTRANSFERASE ACTIVITY AND VESAMICOL BINDING IN RETT-SYNDROME AND IN RATS WITH NUCLEUS BASALIS LESIONS

The decline in choline acetyltransferase activity has been identified previously within the brains of patients with Rett syndrome and Alzhei mer's disease: The level of [H-3]vesamicol binding to a terminal vesic ular acetylcholine transporter is inversely related to the decline in cortical choline acetyltransferase activity in Alzheimer's disease, wh ich may be due to compensatory processes within surviving cholinergic terminals. In order to investigate whether similar cholinergic compens atory processes are present in the Rett syndrome brain and are altered by normal aging, we investigated the density of cholinergic vesicular transporters in (i) the brains of Rett syndrome patients, and (ii) yo ung and old rats with experimentally induced cholinergic cell loss. In Rett syndrome, a significant decline in choline acetyltransferase act ivity within the putamen and thalamus was directly correlated with a d ecline in [H-3]vesamicol binding. In both young and old rats, basal fo rebrain lesions decreased cortical choline acetyltransferase activity significantly, while [H-3]vesamicol binding was unchanged. In contrast to young and old lesioned rats and patients with Alzheimer's disease, cholinergic cells in the brains of patients with Rett syndrome do not compensate for the loss of cholinergic cells by increasing acetylchol ine vesicular storage. (C) 1996 IBRO. Published by Elsevier Science Lt d.