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Glycogen Synthase Kinase-3 Reduces Acetylcholine Level In Striatum Via Disturbing Cellular Distribution Of Choline Acetyltransferase In Cholinergic Interneurons In Rats.
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Neuroscience 2013 Oct;
Authors: Li Zhao, Chang-Biao Chu, Jun-Fa Li, Yu-Tao Yang, Shi-Qin Niu, Wei Qin, Yong-Gang Hao, Qian Dong, Rui Guan, Wen-Li Hu, Yue Wang
Department of Neurobiology and Beijing Institute for Brain Disorders, Capital Medical University, Beijing, China.
Cholinergic interneurons, which provide the main source of acetylcholine in striatum, control the striatal local circuits and deeply involve in pathogenesis of neurodegenerative diseases. Glycogen synthase kinase-3 (GSK-3) is a crucial kinase with diverse fundamental functions and accepted that deregulation of GSK-3 activity also plays important roles in diverse neurodegenerative diseases. However, up to now, there is no direct proof indicating whether GSK-3 activation is responsible for cholinergic dysfunction. In present study, with combined intracerebroventricular injection of Wortmannin and GF-109203X, we activated GSK-3 and demonstrated the increased phosphorylation level of microtubule-associated protein tau and neurofilaments in rat striatum. The activated GSK-3 consequently decreased acetylcholine level in striatum as a result of the reduction of choline acetyltransferase (ChAT) activity. The alteration of ChAT activity was due to impaired ChAT distribution rather than its expression. Furthermore, we proved that cellular ChAT distribution was dependent on low phosphorylation level of neurofilaments. Nevertheless, the cholinergic dysfunction in striatum failed to induce significant neuronal number reduction. In summary, our data demonstrates the link between GSK-3 activation and cholinergic dysfunction in striatum and provided the beneficial evidences for the pathogenesis study of relevant neurodegenerative diseases.
PMID: 24121130 [PubMed - as supplied by publisher]