| Long-term synaptic plasticity is impaired in rats with lesions of the ventrolateral preoptic nucleus. | |
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MedLine Citation:
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PMID: 20128848 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Impairment of memory functions has been frequently reported in models of sleep deprivation. Similarly, hippocampal long-term synaptic plasticity has been shown to be sensitive to sleep loss caused by acute sleep restriction. However, such approaches are limited by the stressful nature of sleep deprivation, and because it is difficult to study long-term sleep restriction in animals. Here, we report the effects of chronic sleep loss on hippocampal long-term potentiation (LTP) in a rodent model of chronic partial sleep deprivation. We studied LTP of the Schaffer collateral-CA1 synapses in hippocampal slices prepared from rats with lesions of the ventrolateral preoptic nucleus (VLPO), which suffered reductions in total sleep time for several weeks after lesions. In slices prepared from VLPO-lesioned rats, LTP was impaired proportionally to the amount of sleep loss, and the decline in LTP followed a single exponential function over the amount of accumulated sleep debt. As compared with sham-lesioned controls, hippocampal slices from VLPO-lesioned rats showed a greater response to adenosine antagonists and greater paired-pulse facilitation (PPF). However, exogenous adenosine depressed evoked synaptic transmission and increased PPF in VLPO-lesioned and sham-lesioned rats by equal amounts, suggesting that the greater endogenous adenosine inhibitory tone in the VLPO-lesioned rats is associated with greater ligand accumulation rather than a change in adenosine receptor sensitivity or adenosine-mediated neurotransmitter release probability. LTP in VLPO-lesioned animals was partially restored by adenosine antagonists, suggesting that adenosine accumulation in VLPO-lesioned animals could account for some of the observed synaptic plasticity deficits. |
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Authors:
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Elda Arrigoni; Jun Lu; Ramalingam Vetrivelan; Clifford B Saper |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, N.I.H., Extramural Date: 2009-11-25 |
Journal Detail:
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Title: The European journal of neuroscience Volume: 30 ISSN: 1460-9568 ISO Abbreviation: Eur. J. Neurosci. Publication Date: 2009 Dec |
Date Detail:
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Created Date: 2010-02-04 Completed Date: 2011-06-06 Revised Date: 2012-11-08 |
Medline Journal Info:
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Nlm Unique ID: 8918110 Medline TA: Eur J Neurosci Country: France |
Other Details:
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Languages: eng Pagination: 2112-20 Citation Subset: IM |
Affiliation:
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Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. earrigon@bidmc.harvard.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Electric Stimulation / methods Electroencephalography Electromyography Excitatory Postsynaptic Potentials / drug effects, physiology Eye Movements / physiology Hippocampus / cytology Male Neural Pathways / physiology Neuronal Plasticity / drug effects, physiology* Preoptic Area / injuries*, physiology* Rats Rats, Sprague-Dawley Receptor, Adenosine A1 / antagonists & inhibitors Sleep / physiology Synapses / drug effects, physiology* Wakefulness / physiology Xanthines / pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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P50 HL060292/HL/NHLBI NIH HHS; P50 HL060292-010003/HL/NHLBI NIH HHS; P50 HL060292-020003/HL/NHLBI NIH HHS; P50 HL060292-030003/HL/NHLBI NIH HHS; P50 HL060292-040003/HL/NHLBI NIH HHS; P50 HL060292-050003/HL/NHLBI NIH HHS; P50-HL60292/HL/NHLBI NIH HHS; R01 NS061863/NS/NINDS NIH HHS; R01 NS061863-01A1/NS/NINDS NIH HHS; R01NS061863/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Receptor, Adenosine A1; 0/Xanthines; 102146-07-6/1,3-dipropyl-8-cyclopentylxanthine |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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