| pubmed-article:15318343 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15318343 | lifeskim:mentions | umls-concept:C0206745 | lld:lifeskim |
| pubmed-article:15318343 | lifeskim:mentions | umls-concept:C0231484 | lld:lifeskim |
| pubmed-article:15318343 | lifeskim:mentions | umls-concept:C0034792 | lld:lifeskim |
| pubmed-article:15318343 | lifeskim:mentions | umls-concept:C0001044 | lld:lifeskim |
| pubmed-article:15318343 | lifeskim:mentions | umls-concept:C0543482 | lld:lifeskim |
| pubmed-article:15318343 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
| pubmed-article:15318343 | lifeskim:mentions | umls-concept:C2258088 | lld:lifeskim |
| pubmed-article:15318343 | lifeskim:mentions | umls-concept:C0599283 | lld:lifeskim |
| pubmed-article:15318343 | lifeskim:mentions | umls-concept:C2732140 | lld:lifeskim |
| pubmed-article:15318343 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:15318343 | pubmed:dateCreated | 2004-8-19 | lld:pubmed |
| pubmed-article:15318343 | pubmed:abstractText | Nerve-evoked contractions were studied in vitro in phrenic nerve-hemidiaphragm preparations from strain 129X1 acetylcholinesterase knockout (AChE-/-) mice and their wild-type littermates (AChE+/+). The AChE-/- mice fail to express AChE but have normal levels of butyrylcholinesterase (BChE) and can survive into adulthood. Twitch tensions elicited in diaphragms of AChE-/- mice by single supramaximal stimuli had larger amplitudes and slower rise and decay times than did those in wild-type animals. In AChE-/- preparations, repetitive stimulation at frequencies of 20 and 50 Hz and at 200 and 400 Hz produced decremental muscle tensions; however, stimulation at 70 and 100 Hz resulted in little or no loss of tension during trains. Muscles from AChE+/+ mice maintained tension at all frequencies examined but exhibited tetanic fade after exposure to the selective AChE inhibitor 1,5-bis(4-allyldimethyl-ammoniumphenyl)pentane-3-one (BW 284C51). The ability of diaphragm muscles from AChE-/- mice to maintain tension at 70 and 100 Hz suggests a partial compensation for impairment of acetylcholine (ACh) hydrolysis. Three mechanisms--including a reliance on BChE activity for termination of ACh action, downregulation of nicotinic acetylcholine receptors (nAChRs), and morphological remodeling of the endplate region--were identified. Studies of neuromuscular transmission in this model system provide an excellent opportunity to evaluate the role of AChE without complications arising from use of inhibitors. | lld:pubmed |
| pubmed-article:15318343 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15318343 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15318343 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15318343 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15318343 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15318343 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15318343 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:15318343 | pubmed:issn | 0148-639X | lld:pubmed |
| pubmed-article:15318343 | pubmed:author | pubmed-author:LockridgeOksa... | lld:pubmed |
| pubmed-article:15318343 | pubmed:author | pubmed-author:OylerGeorgeG | lld:pubmed |
| pubmed-article:15318343 | pubmed:author | pubmed-author:AdlerMichaelM | lld:pubmed |
| pubmed-article:15318343 | pubmed:author | pubmed-author:DuysenEllen... | lld:pubmed |
| pubmed-article:15318343 | pubmed:author | pubmed-author:PurcellAngela... | lld:pubmed |
| pubmed-article:15318343 | pubmed:author | pubmed-author:KanRobert KRK | lld:pubmed |
| pubmed-article:15318343 | pubmed:author | pubmed-author:HamiltonTrace... | lld:pubmed |
| pubmed-article:15318343 | pubmed:author | pubmed-author:ManleyHeather... | lld:pubmed |
| pubmed-article:15318343 | pubmed:author | pubmed-author:DeshpandeShar... | lld:pubmed |
| pubmed-article:15318343 | pubmed:author | pubmed-author:SheridanRober... | lld:pubmed |
| pubmed-article:15318343 | pubmed:copyrightInfo | Copyright 2004 Wiley Periodicals, Inc. | lld:pubmed |
| pubmed-article:15318343 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15318343 | pubmed:volume | 30 | lld:pubmed |
| pubmed-article:15318343 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15318343 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15318343 | pubmed:pagination | 317-27 | lld:pubmed |
| pubmed-article:15318343 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:15318343 | pubmed:meshHeading | pubmed-meshheading:15318343... | lld:pubmed |
| pubmed-article:15318343 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15318343 | pubmed:articleTitle | Reduced acetylcholine receptor density, morphological remodeling, and butyrylcholinesterase activity can sustain muscle function in acetylcholinesterase knockout mice. | lld:pubmed |
| pubmed-article:15318343 | pubmed:affiliation | Neurotoxicology Branch, Pharmacology Division, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Maryland 21010, USA. Michael.Adler@amedd.army.mil | lld:pubmed |
| pubmed-article:15318343 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15318343 | pubmed:publicationType | Comparative Study | lld:pubmed |
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