Differential distribution of butyrylcholinesterase and acetylcholinesterase in the human thalamus
- 10 June 2003
- journal article
- research article
- Published by Wiley in Journal of Comparative Neurology
- Vol. 463 (1) , 25-43
- https://doi.org/10.1002/cne.10751
Abstract
It has been hypothesized that acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) are coregulators of the duration of action of acetylcholine in cholinergic neurotransmission, suggesting that BuChE may also have an important role in the brain. To compare the expression of cholinesterases in the human thalamus, the distributions of BuChE and AChE activity were studied by using a modified Karnovsky-Roots method. BuChE activity was present mainly in neurons, whereas AChE activity was present in both neurons and axons. There was intense staining for BuChE or AChE throughout the thalamus, with some nuclei primarily expressing one or the other cholinesterase. BuChE staining was most intense and widespread in neurons in the anteroventral, mediodorsal, ventral, lateral, and pulvinar thalamic nuclei. AChE was predominantly expressed in neurons of the anterodorsal, midline, ventral, intralaminar, and reticular nuclei. Many nuclei contained both cholinesterases. Considering the overall patterns of labeling in the thalamus for the two cholinesterases, there were both complementary and overlapping relationships of BuChE and AChE activity. Neuronal staining in the subthalamic nucleus and hypothalamus was predominantly positive for AChE activity. The distinct distribution of BuChE activity in neurons in the human thalamus is consistent with an important role for this enzyme in neurotransmission in the human nervous system. Furthermore, BuChE activity, like AChE activity, is found in certain thalamic nuclei related to cognitive and behavioral functions. Involvement of thalamic nuclei in diseases of the nervous system such as Alzheimer's disease and schizophrenia suggests that BuChE could be a potential target for therapeutic intervention in these disorders. J. Comp. Neurol. 463:25–43, 2003.Keywords
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