| Sustaining high acetylcholine levels in the frontal cortex, but not retrosplenial cortex, recovers spatial memory performance in a rodent model of diencephalic amnesia. | |
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MedLine Citation:
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PMID: 22448856 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Although the thalamus and/or mammillary bodies are the primary sites of neuropathology in cases of diencephalic amnesia such as Wernicke Korsakoff Syndrome (WKS), there is also functional deactivation of certain cortical regions that contribute to the cognitive dysfunction. Acetylcholine (ACh) is a key neurotransmitter that modulates neural processing within the cortex and between the thalamus and cortex. In the pyrithiamine-induced thiamine deficiency (PTD) rat model of WKS, there are significant reductions in cholinergic innervation and behaviorally stimulated ACh efflux in the frontal (FC) and retrosplenial (RSC) cortices. In the present study, ACh released levels were site-specifically amplified with physostigmine (0.5 μg, 1.0 μg) in the FC and the RSC, which was confirmed with in vivo microdialysis. Although physostigmine sustained high ACh levels in both cortical regions, the effects on spatial memory, assessed by spontaneous alternation, were different as a function of region (FC, RSC) and treatment (PTD, pair-fed [PF]). Higher ACh levels in the FC recovered the rate of alternation in PTD rats as well as reduced arm-reentry perseverative errors. However, higher ACh levels within the FC of PF rats exacerbated arm-reentry perseverative errors without significantly affecting alternation rates. Maintaining high ACh levels in the RSC had no procognitive effects in PTD rats, but rather impaired alternation behavior in PF rats. These results demonstrate that diverse cortical regions respond differently to intensified ACh levels-and the effects are dependent on thalamic pathology. Thus, pharmacotherapeutics aimed at enhancing cognitive functions must account for the unique features of cortical ACh stimulation and the connective circuitry with the thalamus. |
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Authors:
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Lisa M Savage |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Behavioral neuroscience Volume: 126 ISSN: 1939-0084 ISO Abbreviation: Behav. Neurosci. Publication Date: 2012 Apr |
Date Detail:
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Created Date: 2012-03-27 Completed Date: 2012-07-25 Revised Date: 2013-04-03 |
Medline Journal Info:
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Nlm Unique ID: 8302411 Medline TA: Behav Neurosci Country: United States |
Other Details:
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Languages: eng Pagination: 226-36 Citation Subset: IM |
Copyright Information:
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(c) 2012 APA, all rights reserved |
Affiliation:
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Behavioral Neuroscience Program, Department of Psychology, State University of New York at Binghamton, Binghamton, NY 13902, USA. lsavage@binghamton.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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metabolism* Animals Cerebral Cortex / drug effects, metabolism, physiopathology* Frontal Lobe / drug effects, metabolism, physiopathology* Gyrus Cinguli / drug effects, metabolism, physiopathology* Hippocampus / drug effects Korsakoff Syndrome / metabolism, physiopathology* Maze Learning / drug effects Microdialysis Models, Animal Physostigmine Pyrithiamine Rats Thalamus / drug effects, pathology Thiamine Deficiency / chemically induced |
| Grant Support | |
ID/Acronym/Agency:
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R01 NS054272-01A1/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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51-84-3/Acetylcholine; 534-64-5/Pyrithiamine; 57-47-6/Physostigmine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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