[ 3H]Vesamicol binding in human brain cholinergic deficiency disorders
We measured the binding of the vesicular acetylcholine transport blocker [ 3H]vesamicol (2-[4-phenylpiperidino] cyclohexanol; AH-5183) to autopsied frontal cortex and amygdala of patients from 4 disorders having a marked brain cholinergic reduction, namely Alzheimer's disease, Parkinson's...
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Veröffentlicht in: | Neuroscience letters 1990-09, Vol.117 (3), p.347-352 |
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creator | Kish, Stephen J. Distefano, Linda M. Dozic̆, Slobodan Robitaille, Yves Rajput, Ali Deck, John H.N. Hornykiewicz, Oleh |
description | We measured the binding of the vesicular acetylcholine transport blocker [
3H]vesamicol (2-[4-phenylpiperidino] cyclohexanol; AH-5183) to autopsied frontal cortex and amygdala of patients from 4 disorders having a marked brain cholinergic reduction, namely Alzheimer's disease, Parkinson's disease with dementia, dominantly inherited olivopontocerebellar atrophy and Down's syndrome. Although mean activity of the specific cholinergic marker enzyme choline acetyltransferase (ChAT) was markedly reduced by about 60% in frontal cortex in the 4 patient groups and by 80% or greater in amygdala of the Alzheimer's and Down's syndrome patients, [
3H]vesamicol binding density was, on average, either normal or only slightly reduced as compared with the controls. This discrepancy suggests that in human brain [
3H]vesamicol binding is either not preferentially localized to cholinergic nerve endings or, in these cholinergic deficiency syndromes, a substantial proportion of the vesamicol binding sites persist on cholinergic nerve terminals despite loss of ChAT activity. |
doi_str_mv | 10.1016/0304-3940(90)90689-7 |
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3H]vesamicol (2-[4-phenylpiperidino] cyclohexanol; AH-5183) to autopsied frontal cortex and amygdala of patients from 4 disorders having a marked brain cholinergic reduction, namely Alzheimer's disease, Parkinson's disease with dementia, dominantly inherited olivopontocerebellar atrophy and Down's syndrome. Although mean activity of the specific cholinergic marker enzyme choline acetyltransferase (ChAT) was markedly reduced by about 60% in frontal cortex in the 4 patient groups and by 80% or greater in amygdala of the Alzheimer's and Down's syndrome patients, [
3H]vesamicol binding density was, on average, either normal or only slightly reduced as compared with the controls. This discrepancy suggests that in human brain [
3H]vesamicol binding is either not preferentially localized to cholinergic nerve endings or, in these cholinergic deficiency syndromes, a substantial proportion of the vesamicol binding sites persist on cholinergic nerve terminals despite loss of ChAT activity.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/0304-3940(90)90689-7</identifier><identifier>PMID: 2151294</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>[ 3H]Vesamicol ; Acetylcholine ; Acetylcholine - metabolism ; Adult ; Aged ; AH-5183 ; Alzheimer Disease - metabolism ; Alzheimer's disease ; Amygdala - metabolism ; Autonomic Nervous System Diseases - metabolism ; Biological and medical sciences ; Brain ; Brain Chemistry ; Cerebral Cortex - metabolism ; Choline acetyltransferase ; Choline O-Acetyltransferase - metabolism ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Down Syndrome - metabolism ; Humans ; Medical sciences ; Middle Aged ; Neurology ; Neuromuscular Depolarizing Agents - metabolism ; Olivopontocerebellar Atrophies - metabolism ; Parasympathetic Nervous System - metabolism ; Parkinson Disease - metabolism ; Piperidines - metabolism</subject><ispartof>Neuroscience letters, 1990-09, Vol.117 (3), p.347-352</ispartof><rights>1990</rights><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-81d035b011a51c129f2223a93a6310d7bcbcdf126b1d36325a5bb0f4db857c953</citedby><cites>FETCH-LOGICAL-c387t-81d035b011a51c129f2223a93a6310d7bcbcdf126b1d36325a5bb0f4db857c953</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0304-3940(90)90689-7$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19432260$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2151294$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kish, Stephen J.</creatorcontrib><creatorcontrib>Distefano, Linda M.</creatorcontrib><creatorcontrib>Dozic̆, Slobodan</creatorcontrib><creatorcontrib>Robitaille, Yves</creatorcontrib><creatorcontrib>Rajput, Ali</creatorcontrib><creatorcontrib>Deck, John H.N.</creatorcontrib><creatorcontrib>Hornykiewicz, Oleh</creatorcontrib><title>[ 3H]Vesamicol binding in human brain cholinergic deficiency disorders</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>We measured the binding of the vesicular acetylcholine transport blocker [
3H]vesamicol (2-[4-phenylpiperidino] cyclohexanol; AH-5183) to autopsied frontal cortex and amygdala of patients from 4 disorders having a marked brain cholinergic reduction, namely Alzheimer's disease, Parkinson's disease with dementia, dominantly inherited olivopontocerebellar atrophy and Down's syndrome. Although mean activity of the specific cholinergic marker enzyme choline acetyltransferase (ChAT) was markedly reduced by about 60% in frontal cortex in the 4 patient groups and by 80% or greater in amygdala of the Alzheimer's and Down's syndrome patients, [
3H]vesamicol binding density was, on average, either normal or only slightly reduced as compared with the controls. This discrepancy suggests that in human brain [
3H]vesamicol binding is either not preferentially localized to cholinergic nerve endings or, in these cholinergic deficiency syndromes, a substantial proportion of the vesamicol binding sites persist on cholinergic nerve terminals despite loss of ChAT activity.</description><subject>[ 3H]Vesamicol</subject><subject>Acetylcholine</subject><subject>Acetylcholine - metabolism</subject><subject>Adult</subject><subject>Aged</subject><subject>AH-5183</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer's disease</subject><subject>Amygdala - metabolism</subject><subject>Autonomic Nervous System Diseases - metabolism</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Brain Chemistry</subject><subject>Cerebral Cortex - metabolism</subject><subject>Choline acetyltransferase</subject><subject>Choline O-Acetyltransferase - metabolism</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Down Syndrome - metabolism</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Neuromuscular Depolarizing Agents - metabolism</subject><subject>Olivopontocerebellar Atrophies - metabolism</subject><subject>Parasympathetic Nervous System - metabolism</subject><subject>Parkinson Disease - metabolism</subject><subject>Piperidines - metabolism</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtKxTAQhoMoejz6BgrdKLqoTpKmaTaCHLyB4EbdiITcqpFeNDkVfHtTT9GdMDAD883P8CG0h-EEAy5PgUKRU1HAkYBjAWUlcr6GZrjiJOeCk3U0-0W20HaMbwDAMCs20SbBDBNRzNDlU0avnx9dVK03fZNp31nfvWS-y16HVnWZDirN5rVvfOfCizeZdbU33nXmK7M-9sG6EHfQRq2a6HanPkcPlxf3i-v89u7qZnF-mxta8WVeYQuUacBYMWzSBzUhhCpBVUkxWK6NNrbGpNTY0pISppjWUBdWV4wbwegcHa5y30P_Mbi4lK2PxjWN6lw_RFkBLYqK4wQWK9CEPsbgavkefKvCl8QgR31ydCNHN1KMlfRJns72p_xBt87-Hk2-0v5g2qtoVFMH1Rkf_7ITQkgJiTtbcS7J-PQuyPijzFkfnFlK2_v_H_kGPBSKgA</recordid><startdate>19900918</startdate><enddate>19900918</enddate><creator>Kish, Stephen J.</creator><creator>Distefano, Linda M.</creator><creator>Dozic̆, Slobodan</creator><creator>Robitaille, Yves</creator><creator>Rajput, Ali</creator><creator>Deck, John H.N.</creator><creator>Hornykiewicz, Oleh</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19900918</creationdate><title>[ 3H]Vesamicol binding in human brain cholinergic deficiency disorders</title><author>Kish, Stephen J. ; Distefano, Linda M. ; Dozic̆, Slobodan ; Robitaille, Yves ; Rajput, Ali ; Deck, John H.N. ; Hornykiewicz, Oleh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-81d035b011a51c129f2223a93a6310d7bcbcdf126b1d36325a5bb0f4db857c953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>[ 3H]Vesamicol</topic><topic>Acetylcholine</topic><topic>Acetylcholine - metabolism</topic><topic>Adult</topic><topic>Aged</topic><topic>AH-5183</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer's disease</topic><topic>Amygdala - metabolism</topic><topic>Autonomic Nervous System Diseases - metabolism</topic><topic>Biological and medical sciences</topic><topic>Brain</topic><topic>Brain Chemistry</topic><topic>Cerebral Cortex - metabolism</topic><topic>Choline acetyltransferase</topic><topic>Choline O-Acetyltransferase - metabolism</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Down Syndrome - metabolism</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Neuromuscular Depolarizing Agents - metabolism</topic><topic>Olivopontocerebellar Atrophies - metabolism</topic><topic>Parasympathetic Nervous System - metabolism</topic><topic>Parkinson Disease - metabolism</topic><topic>Piperidines - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kish, Stephen J.</creatorcontrib><creatorcontrib>Distefano, Linda M.</creatorcontrib><creatorcontrib>Dozic̆, Slobodan</creatorcontrib><creatorcontrib>Robitaille, Yves</creatorcontrib><creatorcontrib>Rajput, Ali</creatorcontrib><creatorcontrib>Deck, John H.N.</creatorcontrib><creatorcontrib>Hornykiewicz, Oleh</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kish, Stephen J.</au><au>Distefano, Linda M.</au><au>Dozic̆, Slobodan</au><au>Robitaille, Yves</au><au>Rajput, Ali</au><au>Deck, John H.N.</au><au>Hornykiewicz, Oleh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>[ 3H]Vesamicol binding in human brain cholinergic deficiency disorders</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>1990-09-18</date><risdate>1990</risdate><volume>117</volume><issue>3</issue><spage>347</spage><epage>352</epage><pages>347-352</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><coden>NELED5</coden><abstract>We measured the binding of the vesicular acetylcholine transport blocker [
3H]vesamicol (2-[4-phenylpiperidino] cyclohexanol; AH-5183) to autopsied frontal cortex and amygdala of patients from 4 disorders having a marked brain cholinergic reduction, namely Alzheimer's disease, Parkinson's disease with dementia, dominantly inherited olivopontocerebellar atrophy and Down's syndrome. Although mean activity of the specific cholinergic marker enzyme choline acetyltransferase (ChAT) was markedly reduced by about 60% in frontal cortex in the 4 patient groups and by 80% or greater in amygdala of the Alzheimer's and Down's syndrome patients, [
3H]vesamicol binding density was, on average, either normal or only slightly reduced as compared with the controls. This discrepancy suggests that in human brain [
3H]vesamicol binding is either not preferentially localized to cholinergic nerve endings or, in these cholinergic deficiency syndromes, a substantial proportion of the vesamicol binding sites persist on cholinergic nerve terminals despite loss of ChAT activity.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>2151294</pmid><doi>10.1016/0304-3940(90)90689-7</doi><tpages>6</tpages></addata></record> |
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subjects | [ 3H]Vesamicol Acetylcholine Acetylcholine - metabolism Adult Aged AH-5183 Alzheimer Disease - metabolism Alzheimer's disease Amygdala - metabolism Autonomic Nervous System Diseases - metabolism Biological and medical sciences Brain Brain Chemistry Cerebral Cortex - metabolism Choline acetyltransferase Choline O-Acetyltransferase - metabolism Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Down Syndrome - metabolism Humans Medical sciences Middle Aged Neurology Neuromuscular Depolarizing Agents - metabolism Olivopontocerebellar Atrophies - metabolism Parasympathetic Nervous System - metabolism Parkinson Disease - metabolism Piperidines - metabolism |
title | [ 3H]Vesamicol binding in human brain cholinergic deficiency disorders |
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