Striatal presynaptic dopamine function in type 1 alcoholics measured with positron emission tomography
Recent in vivo studies have shown low dopamine D 2 receptor and dopamine transporter densities among late onset (type 1) alcoholics. We have now studied 6-[ 18 F]-FDOPA (FDOPA) uptake in 10 type 1 alcoholics and eight matched controls to test the hypothesis that striatal presynaptic dopamine functio...
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creator | Tiihonen, J Vilkman, H Räsänen, P Ryynänen, O-P Hakko, H Bergman, J Hämäläinen, T Laakso, A Haaparanta-Solin, M Solin, O Kuoppamäki, M Syvälahti, E Hietala, J |
description | Recent
in vivo
studies have shown low dopamine D
2
receptor and dopamine transporter densities among late onset (type 1) alcoholics. We have now studied 6-[
18
F]-FDOPA (FDOPA) uptake in 10 type 1 alcoholics and eight matched controls to test the hypothesis that striatal presynaptic dopamine function is lower among alcoholics. Markedly low FDOPA uptake (K
i
) was observed in the left caudate of two alcoholic patients, but the mean striatal uptake values of the patient group were higher than those of the control group. The greatest difference was observed in the mean FDOPA intake in the left putamen, which was 28% higher in the patient group (
t
= 3.00,
P
= 0.008, d.f. = 16, independent samples
t
-test), and in the right caudate (difference 36%,
t
= 2.87,
P
= 0.01). The elevated FDOPA uptake in putamen and caudate correlated with poor Wisconsin Card Sorting Test (WCST) performance (error %) among alcoholics (correlation coefficients from 0.49 to 0.56), which suggests that the magnitude of presynaptic dopamine function alteration correlates with the degree of disability to modify one's behavior. The results do not give support to the hypothesis of generally decreased striatal dopamine turnover in type 1 alcoholism, but on the contrary indicate an increased presynaptic dopamine function. This may represent a compensatory mechanism to low postsynaptic DA function. The low presynaptic DA function observed in the left caudate of two patients suggests that type 1 alcoholism may be a heterogeneous disorder. |
doi_str_mv | 10.1038/sj.mp.4000365 |
format | Article |
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in vivo
studies have shown low dopamine D
2
receptor and dopamine transporter densities among late onset (type 1) alcoholics. We have now studied 6-[
18
F]-FDOPA (FDOPA) uptake in 10 type 1 alcoholics and eight matched controls to test the hypothesis that striatal presynaptic dopamine function is lower among alcoholics. Markedly low FDOPA uptake (K
i
) was observed in the left caudate of two alcoholic patients, but the mean striatal uptake values of the patient group were higher than those of the control group. The greatest difference was observed in the mean FDOPA intake in the left putamen, which was 28% higher in the patient group (
t
= 3.00,
P
= 0.008, d.f. = 16, independent samples
t
-test), and in the right caudate (difference 36%,
t
= 2.87,
P
= 0.01). The elevated FDOPA uptake in putamen and caudate correlated with poor Wisconsin Card Sorting Test (WCST) performance (error %) among alcoholics (correlation coefficients from 0.49 to 0.56), which suggests that the magnitude of presynaptic dopamine function alteration correlates with the degree of disability to modify one's behavior. The results do not give support to the hypothesis of generally decreased striatal dopamine turnover in type 1 alcoholism, but on the contrary indicate an increased presynaptic dopamine function. This may represent a compensatory mechanism to low postsynaptic DA function. The low presynaptic DA function observed in the left caudate of two patients suggests that type 1 alcoholism may be a heterogeneous disorder.</description><identifier>ISSN: 1359-4184</identifier><identifier>EISSN: 1476-5578</identifier><identifier>DOI: 10.1038/sj.mp.4000365</identifier><identifier>PMID: 9577840</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Addictive behaviors ; Adult ; Adult and adolescent clinical studies ; Alcoholics ; Alcoholism ; Alcoholism - classification ; Alcoholism - diagnostic imaging ; Alcoholism - metabolism ; Behavioral Sciences ; Biological and medical sciences ; Biological Psychology ; Carrier Proteins - physiology ; Caudate Nucleus - diagnostic imaging ; Caudate Nucleus - metabolism ; Corpus Striatum - diagnostic imaging ; Corpus Striatum - metabolism ; Dihydroxyphenylalanine - analogs & derivatives ; Dihydroxyphenylalanine - pharmacokinetics ; Dominance, Cerebral ; Dopamine ; Dopamine - physiology ; Dopamine D2 receptors ; Dopamine Plasma Membrane Transport Proteins ; Dopamine transporter ; Finland ; Fluorine Radioisotopes - pharmacokinetics ; Humans ; Hypotheses ; Magnetic Resonance Imaging ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Membrane Glycoproteins ; Membrane Transport Proteins ; Middle Aged ; Models, Neurological ; Models, Psychological ; Neostriatum ; Nerve Tissue Proteins ; Neuropsychological Tests ; Neurosciences ; original-research-article ; Pharmacotherapy ; Positron emission tomography ; Presynaptic Terminals - metabolism ; Psychiatry ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Putamen ; Putamen - diagnostic imaging ; Putamen - metabolism ; Receptors, Dopamine D2 - physiology ; Tomography, Emission-Computed</subject><ispartof>Molecular psychiatry, 1998-03, Vol.3 (2), p.156-161</ispartof><rights>Macmillan Publishers Limited 1998</rights><rights>1999 INIST-CNRS</rights><rights>Macmillan Publishers Limited 1998.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c437t-7d412de0ece8c11f26ea20b0ea6a43efeb28b3416b6ce6c8e98a058316037ba13</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.mp.4000365$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.mp.4000365$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1871363$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9577840$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tiihonen, J</creatorcontrib><creatorcontrib>Vilkman, H</creatorcontrib><creatorcontrib>Räsänen, P</creatorcontrib><creatorcontrib>Ryynänen, O-P</creatorcontrib><creatorcontrib>Hakko, H</creatorcontrib><creatorcontrib>Bergman, J</creatorcontrib><creatorcontrib>Hämäläinen, T</creatorcontrib><creatorcontrib>Laakso, A</creatorcontrib><creatorcontrib>Haaparanta-Solin, M</creatorcontrib><creatorcontrib>Solin, O</creatorcontrib><creatorcontrib>Kuoppamäki, M</creatorcontrib><creatorcontrib>Syvälahti, E</creatorcontrib><creatorcontrib>Hietala, J</creatorcontrib><title>Striatal presynaptic dopamine function in type 1 alcoholics measured with positron emission tomography</title><title>Molecular psychiatry</title><addtitle>Mol Psychiatry</addtitle><addtitle>Mol Psychiatry</addtitle><description>Recent
in vivo
studies have shown low dopamine D
2
receptor and dopamine transporter densities among late onset (type 1) alcoholics. We have now studied 6-[
18
F]-FDOPA (FDOPA) uptake in 10 type 1 alcoholics and eight matched controls to test the hypothesis that striatal presynaptic dopamine function is lower among alcoholics. Markedly low FDOPA uptake (K
i
) was observed in the left caudate of two alcoholic patients, but the mean striatal uptake values of the patient group were higher than those of the control group. The greatest difference was observed in the mean FDOPA intake in the left putamen, which was 28% higher in the patient group (
t
= 3.00,
P
= 0.008, d.f. = 16, independent samples
t
-test), and in the right caudate (difference 36%,
t
= 2.87,
P
= 0.01). The elevated FDOPA uptake in putamen and caudate correlated with poor Wisconsin Card Sorting Test (WCST) performance (error %) among alcoholics (correlation coefficients from 0.49 to 0.56), which suggests that the magnitude of presynaptic dopamine function alteration correlates with the degree of disability to modify one's behavior. The results do not give support to the hypothesis of generally decreased striatal dopamine turnover in type 1 alcoholism, but on the contrary indicate an increased presynaptic dopamine function. This may represent a compensatory mechanism to low postsynaptic DA function. The low presynaptic DA function observed in the left caudate of two patients suggests that type 1 alcoholism may be a heterogeneous disorder.</description><subject>Addictive behaviors</subject><subject>Adult</subject><subject>Adult and adolescent clinical studies</subject><subject>Alcoholics</subject><subject>Alcoholism</subject><subject>Alcoholism - classification</subject><subject>Alcoholism - diagnostic imaging</subject><subject>Alcoholism - metabolism</subject><subject>Behavioral Sciences</subject><subject>Biological and medical sciences</subject><subject>Biological Psychology</subject><subject>Carrier Proteins - physiology</subject><subject>Caudate Nucleus - diagnostic imaging</subject><subject>Caudate Nucleus - metabolism</subject><subject>Corpus Striatum - diagnostic imaging</subject><subject>Corpus Striatum - metabolism</subject><subject>Dihydroxyphenylalanine - analogs & derivatives</subject><subject>Dihydroxyphenylalanine - pharmacokinetics</subject><subject>Dominance, Cerebral</subject><subject>Dopamine</subject><subject>Dopamine - physiology</subject><subject>Dopamine D2 receptors</subject><subject>Dopamine Plasma Membrane Transport Proteins</subject><subject>Dopamine transporter</subject><subject>Finland</subject><subject>Fluorine Radioisotopes - pharmacokinetics</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Membrane Glycoproteins</subject><subject>Membrane Transport Proteins</subject><subject>Middle Aged</subject><subject>Models, Neurological</subject><subject>Models, Psychological</subject><subject>Neostriatum</subject><subject>Nerve Tissue Proteins</subject><subject>Neuropsychological Tests</subject><subject>Neurosciences</subject><subject>original-research-article</subject><subject>Pharmacotherapy</subject><subject>Positron emission tomography</subject><subject>Presynaptic Terminals - metabolism</subject><subject>Psychiatry</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Putamen</subject><subject>Putamen - diagnostic imaging</subject><subject>Putamen - metabolism</subject><subject>Receptors, Dopamine D2 - physiology</subject><subject>Tomography, Emission-Computed</subject><issn>1359-4184</issn><issn>1476-5578</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkM2LFDEQxYMo67p69CgEFG89Jp3POcriFyx4UM8hna7eydCdxCTNMv-9GaZxQTxVwfvVq8dD6DUlO0qY_lCOuyXtOCGESfEEXVOuZCeE0k_bzsS-41Tz5-hFKUdCzqK4Qld7oZTm5BpNP2r2ttoZpwzlFGyq3uExJrv4AHhag6s-BuwDrqcEmGI7u3iIs3cFL2DLmmHED74ecIrF19xYWHwp56Mal3ifbTqcXqJnk50LvNrmDfr1-dPP26_d3fcv324_3nWOM1U7NXLaj0DAgXaUTr0E25OBgJWWM5hg6PXAOJWDdCCdhr22RGhGJWFqsJTdoPcX35Tj7xVKNS2Lg3m2AeJaDJVcMK5YA9_-Ax7jmkPLZvrGKNE8ZaO6C-VyLCXDZFL2i80nQ4k5t2_K0SzJbO03_s3mug4LjH_pre6mv9t0W5ydp2yD8-XRVCvK5Dnc7oKVpoR7yI_h_v_3D2FAnpA</recordid><startdate>19980301</startdate><enddate>19980301</enddate><creator>Tiihonen, J</creator><creator>Vilkman, H</creator><creator>Räsänen, P</creator><creator>Ryynänen, O-P</creator><creator>Hakko, H</creator><creator>Bergman, J</creator><creator>Hämäläinen, T</creator><creator>Laakso, A</creator><creator>Haaparanta-Solin, M</creator><creator>Solin, O</creator><creator>Kuoppamäki, M</creator><creator>Syvälahti, E</creator><creator>Hietala, J</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>7TK</scope><scope>K9.</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>19980301</creationdate><title>Striatal presynaptic dopamine function in type 1 alcoholics measured with positron emission tomography</title><author>Tiihonen, J ; Vilkman, H ; Räsänen, P ; Ryynänen, O-P ; Hakko, H ; Bergman, J ; Hämäläinen, T ; Laakso, A ; Haaparanta-Solin, M ; Solin, O ; Kuoppamäki, M ; Syvälahti, E ; Hietala, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c437t-7d412de0ece8c11f26ea20b0ea6a43efeb28b3416b6ce6c8e98a058316037ba13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Addictive behaviors</topic><topic>Adult</topic><topic>Adult and adolescent clinical studies</topic><topic>Alcoholics</topic><topic>Alcoholism</topic><topic>Alcoholism - classification</topic><topic>Alcoholism - diagnostic imaging</topic><topic>Alcoholism - metabolism</topic><topic>Behavioral Sciences</topic><topic>Biological and medical sciences</topic><topic>Biological Psychology</topic><topic>Carrier Proteins - physiology</topic><topic>Caudate Nucleus - diagnostic imaging</topic><topic>Caudate Nucleus - metabolism</topic><topic>Corpus Striatum - diagnostic imaging</topic><topic>Corpus Striatum - metabolism</topic><topic>Dihydroxyphenylalanine - analogs & derivatives</topic><topic>Dihydroxyphenylalanine - pharmacokinetics</topic><topic>Dominance, Cerebral</topic><topic>Dopamine</topic><topic>Dopamine - physiology</topic><topic>Dopamine D2 receptors</topic><topic>Dopamine Plasma Membrane Transport Proteins</topic><topic>Dopamine transporter</topic><topic>Finland</topic><topic>Fluorine Radioisotopes - pharmacokinetics</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Membrane Glycoproteins</topic><topic>Membrane Transport Proteins</topic><topic>Middle Aged</topic><topic>Models, Neurological</topic><topic>Models, Psychological</topic><topic>Neostriatum</topic><topic>Nerve Tissue Proteins</topic><topic>Neuropsychological Tests</topic><topic>Neurosciences</topic><topic>original-research-article</topic><topic>Pharmacotherapy</topic><topic>Positron emission tomography</topic><topic>Presynaptic Terminals - metabolism</topic><topic>Psychiatry</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Putamen</topic><topic>Putamen - diagnostic imaging</topic><topic>Putamen - metabolism</topic><topic>Receptors, Dopamine D2 - physiology</topic><topic>Tomography, Emission-Computed</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tiihonen, J</creatorcontrib><creatorcontrib>Vilkman, H</creatorcontrib><creatorcontrib>Räsänen, P</creatorcontrib><creatorcontrib>Ryynänen, O-P</creatorcontrib><creatorcontrib>Hakko, H</creatorcontrib><creatorcontrib>Bergman, J</creatorcontrib><creatorcontrib>Hämäläinen, T</creatorcontrib><creatorcontrib>Laakso, A</creatorcontrib><creatorcontrib>Haaparanta-Solin, M</creatorcontrib><creatorcontrib>Solin, O</creatorcontrib><creatorcontrib>Kuoppamäki, M</creatorcontrib><creatorcontrib>Syvälahti, E</creatorcontrib><creatorcontrib>Hietala, J</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>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Molecular psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tiihonen, J</au><au>Vilkman, H</au><au>Räsänen, P</au><au>Ryynänen, O-P</au><au>Hakko, H</au><au>Bergman, J</au><au>Hämäläinen, T</au><au>Laakso, A</au><au>Haaparanta-Solin, M</au><au>Solin, O</au><au>Kuoppamäki, M</au><au>Syvälahti, E</au><au>Hietala, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Striatal presynaptic dopamine function in type 1 alcoholics measured with positron emission tomography</atitle><jtitle>Molecular psychiatry</jtitle><stitle>Mol Psychiatry</stitle><addtitle>Mol Psychiatry</addtitle><date>1998-03-01</date><risdate>1998</risdate><volume>3</volume><issue>2</issue><spage>156</spage><epage>161</epage><pages>156-161</pages><issn>1359-4184</issn><eissn>1476-5578</eissn><abstract>Recent
in vivo
studies have shown low dopamine D
2
receptor and dopamine transporter densities among late onset (type 1) alcoholics. We have now studied 6-[
18
F]-FDOPA (FDOPA) uptake in 10 type 1 alcoholics and eight matched controls to test the hypothesis that striatal presynaptic dopamine function is lower among alcoholics. Markedly low FDOPA uptake (K
i
) was observed in the left caudate of two alcoholic patients, but the mean striatal uptake values of the patient group were higher than those of the control group. The greatest difference was observed in the mean FDOPA intake in the left putamen, which was 28% higher in the patient group (
t
= 3.00,
P
= 0.008, d.f. = 16, independent samples
t
-test), and in the right caudate (difference 36%,
t
= 2.87,
P
= 0.01). The elevated FDOPA uptake in putamen and caudate correlated with poor Wisconsin Card Sorting Test (WCST) performance (error %) among alcoholics (correlation coefficients from 0.49 to 0.56), which suggests that the magnitude of presynaptic dopamine function alteration correlates with the degree of disability to modify one's behavior. The results do not give support to the hypothesis of generally decreased striatal dopamine turnover in type 1 alcoholism, but on the contrary indicate an increased presynaptic dopamine function. This may represent a compensatory mechanism to low postsynaptic DA function. The low presynaptic DA function observed in the left caudate of two patients suggests that type 1 alcoholism may be a heterogeneous disorder.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>9577840</pmid><doi>10.1038/sj.mp.4000365</doi><tpages>6</tpages></addata></record> |
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subjects | Addictive behaviors Adult Adult and adolescent clinical studies Alcoholics Alcoholism Alcoholism - classification Alcoholism - diagnostic imaging Alcoholism - metabolism Behavioral Sciences Biological and medical sciences Biological Psychology Carrier Proteins - physiology Caudate Nucleus - diagnostic imaging Caudate Nucleus - metabolism Corpus Striatum - diagnostic imaging Corpus Striatum - metabolism Dihydroxyphenylalanine - analogs & derivatives Dihydroxyphenylalanine - pharmacokinetics Dominance, Cerebral Dopamine Dopamine - physiology Dopamine D2 receptors Dopamine Plasma Membrane Transport Proteins Dopamine transporter Finland Fluorine Radioisotopes - pharmacokinetics Humans Hypotheses Magnetic Resonance Imaging Male Medical sciences Medicine Medicine & Public Health Membrane Glycoproteins Membrane Transport Proteins Middle Aged Models, Neurological Models, Psychological Neostriatum Nerve Tissue Proteins Neuropsychological Tests Neurosciences original-research-article Pharmacotherapy Positron emission tomography Presynaptic Terminals - metabolism Psychiatry Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Putamen Putamen - diagnostic imaging Putamen - metabolism Receptors, Dopamine D2 - physiology Tomography, Emission-Computed |
title | Striatal presynaptic dopamine function in type 1 alcoholics measured with positron emission tomography |
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