pubmed-article:12645036 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12645036 | lifeskim:mentions | umls-concept:C0001041 | lld:lifeskim |
pubmed-article:12645036 | lifeskim:mentions | umls-concept:C0034830 | lld:lifeskim |
pubmed-article:12645036 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
pubmed-article:12645036 | lifeskim:mentions | umls-concept:C1167622 | lld:lifeskim |
pubmed-article:12645036 | lifeskim:mentions | umls-concept:C0040399 | lld:lifeskim |
pubmed-article:12645036 | lifeskim:mentions | umls-concept:C1621296 | lld:lifeskim |
pubmed-article:12645036 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:12645036 | pubmed:dateCreated | 2003-3-19 | lld:pubmed |
pubmed-article:12645036 | pubmed:abstractText | Although in vitro theory indicates that ligand binding is sensitive to competition with neurotransmitters, only some imaging ligands have shown such competition in vivo. The purpose of this study was to determine whether increases in acetylcholine (ACh) levels induced by an acetylcholinesterase inhibitor, physostigmine, inhibit in vivo binding of [(123)I]5-iodo-3-(2(S)-2-azetidinyl-methoxy) pyridine (5-I-A-85380), a single photon emission computed tomography ligand for the high-affinity type nicotinic ACh receptor (nAChR). Baboons were used for seven studies with a bolus plus constant infusion equilibrium paradigm. After achieving equilibrium at 5 h, physostigmine (0.02 (n = 1), 0.067 (n = 3), and 0.2 (n = 3) mg/kg) was administered intravenously and data were acquired for up to 8 h. To confirm equilibrium conditions, [(123)I]5-I-A-85380 plasma levels were measured in four studies, including all studies with 0.2 mg/kg physostigmine. Prior to physostigmine administration, thalamic activities were stable, with changes of 1.1%/h or less, except in one study with a gradual increase of 4.2%/h. Thalamic activities were decreased by 15% in one study with 0.067 mg/kg and 14-17% in all studies with 0.2 mg/kg physostigmine administration (P = 0.009). In these studies with 0.2 mg/kg physostigmine administration, [(123)I]5-I-A-85380 plasma levels showed a transient or a sustained increase after physostigmine administration that would have increased thalamic activities. These results suggest that elevated ACh levels induced by physostigmine can effectively compete in vivo with [(123)I]5-I-A-85380 binding at nAChRs. However, decreased thalamic activities could have been caused by other mechanisms, including internalization of the receptor with an associated decreased affinity for radioligand. | lld:pubmed |
pubmed-article:12645036 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12645036 | pubmed:language | eng | lld:pubmed |
pubmed-article:12645036 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12645036 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:12645036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12645036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12645036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12645036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12645036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12645036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12645036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12645036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12645036 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12645036 | pubmed:month | Jun | lld:pubmed |
pubmed-article:12645036 | pubmed:issn | 0887-4476 | lld:pubmed |
pubmed-article:12645036 | pubmed:author | pubmed-author:FujitaMasahir... | lld:pubmed |
pubmed-article:12645036 | pubmed:author | pubmed-author:ZoghbiSami... | lld:pubmed |
pubmed-article:12645036 | pubmed:author | pubmed-author:BaldwinRonald... | lld:pubmed |
pubmed-article:12645036 | pubmed:author | pubmed-author:InnisRobert... | lld:pubmed |
pubmed-article:12645036 | pubmed:author | pubmed-author:TamagnanGille... | lld:pubmed |
pubmed-article:12645036 | pubmed:author | pubmed-author:BozkurtAliA | lld:pubmed |
pubmed-article:12645036 | pubmed:author | pubmed-author:Al-TikritiMoh... | lld:pubmed |
pubmed-article:12645036 | pubmed:copyrightInfo | Copyright 2003 Wiley-Liss, Inc. | lld:pubmed |
pubmed-article:12645036 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12645036 | pubmed:day | 1 | lld:pubmed |
pubmed-article:12645036 | pubmed:volume | 48 | lld:pubmed |
pubmed-article:12645036 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12645036 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12645036 | pubmed:pagination | 116-22 | lld:pubmed |
pubmed-article:12645036 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:12645036 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12645036 | pubmed:articleTitle | Influence of acetylcholine levels on the binding of a SPECT nicotinic acetylcholine receptor ligand [123I]5-I-A-85380. | lld:pubmed |
pubmed-article:12645036 | pubmed:affiliation | Department of Psychiatry, Yale University and VA Connecticut HCS, West Haven, Connecticut, USA. FujitaM@intra.nimh.nih.gov | lld:pubmed |
pubmed-article:12645036 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12645036 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:12645036 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:12645036 | lld:pubmed |