L‐Dihydroxyphenylalanine and its decarboxylase: New ideas on their neuroregulatory roles
Identifieur interne : 005873 ( Main/Exploration ); précédent : 005872; suivant : 005874L‐Dihydroxyphenylalanine and its decarboxylase: New ideas on their neuroregulatory roles
Auteurs : Opacka‐Juffry [Royaume-Uni] ; David J. Brooks [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 1995-05.
English descriptors
- KwdEn :
- 6‐[18F]fluoro‐L‐dihydroxyphenylalanine, Animals, Brain (physiopathology), Brain Mapping, Corpus Striatum (physiology), Dihydroxyphenylalanine (physiology), Dopa Decarboxylase (physiology), Dopamine (physiology), Humans, L‐Dihydroxyphenylalanine, L‐Dihydroxyphenylalanine decarboxylase, Neurotransmitter Agents (physiology), Parkinson Disease (physiopathology), Parkinson's disease, Positron emission tomography, Synaptic Transmission (physiology), Tomography, Emission-Computed.
- MESH :
- chemical , physiology : Dihydroxyphenylalanine, Dopa Decarboxylase, Dopamine, Neurotransmitter Agents.
- physiology : Corpus Striatum, Synaptic Transmission.
- physiopathology : Brain, Parkinson Disease.
- Animals, Brain Mapping, Humans, Tomography, Emission-Computed.
Abstract
Recent experimental reports concerning L‐dihydroxyphenylalanine (L‐DOPA) and aromatic L‐amino acid decarboxylase (AADC, L‐DOPA decarboxylase) are reviewed in this article. Both in vitro and in vivo data now suggest that L‐DOPA is an endogenous neuroactive compound that is released from neurons and acts as a neurotransmitter or neuromodulator in the brain. Administration of exogenous L‐DOPA affects dopamine receptor status, AADC activity, and mitochondrial oxidation in experimental animals. The type and severity of these effects depend on the duration of the treatment. These findings may partly explain the limited efficacy of L‐DOPA therapy in Parkinson's disease (PD). AADC also plays a controlling role in the central nervous system, being a regulatory enzyme in the synthesis of a putative neuromodulator 2‐phenylethylamine and other trace amines. Recent experimental findings on AADC activity and localisation are of importance because they suggest that striatal [18F]DOPA uptake used as an indicator of PD progression in positron emission tomography (PET) studies is likely to overestimate nigrostriatal integrity in advanced PD. Possible new PET tracers of presynaptic dopaminergic function are discussed in this context.
Url:
DOI: 10.1002/mds.870100302
Affiliations:
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Brooks</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:9A19ED18260D57A788A678BAC07237BB843FA4EE</idno><date when="1995" year="1995">1995</date><idno type="doi">10.1002/mds.870100302</idno><idno type="url">https://api.istex.fr/document/9A19ED18260D57A788A678BAC07237BB843FA4EE/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000950</idno><idno type="wicri:Area/Istex/Curation">000950</idno><idno type="wicri:Area/Istex/Checkpoint">003D04</idno><idno type="wicri:doubleKey">0885-3185:1995:Opacka Uffry:l:dihydroxyphenylalanine:and</idno><idno type="wicri:source">PubMed</idno><idno type="RBID">pubmed:7651438</idno><idno type="wicri:Area/PubMed/Corpus">004995</idno><idno type="wicri:Area/PubMed/Curation">004995</idno><idno type="wicri:Area/PubMed/Checkpoint">004965</idno><idno type="wicri:Area/Ncbi/Merge">004717</idno><idno type="wicri:Area/Ncbi/Curation">004717</idno><idno type="wicri:Area/Ncbi/Checkpoint">004717</idno><idno type="wicri:doubleKey">0885-3185:1995:Opacka Juffry J:l:dihydroxyphenylalanine:and</idno><idno type="wicri:Area/Main/Merge">008A35</idno><idno type="wicri:Area/Main/Curation">005873</idno><idno type="wicri:Area/Main/Exploration">005873</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">L‐Dihydroxyphenylalanine and its decarboxylase: New ideas on their neuroregulatory roles</title><author><name sortKey="Opacka Uffry" sort="Opacka Uffry" uniqKey="Opacka Uffry" last="Opacka-Juffry">Opacka‐Juffry</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>MRC Cyclotron Unit, Clinical Sciences Centre, Hammersmith Hospital, Queen Square, London</wicri:cityArea></affiliation></author><author><name sortKey="Brooks, David J" sort="Brooks, David J" uniqKey="Brooks D" first="David J." last="Brooks">David J. Brooks</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Institute of Neurology, Queen Square, London</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1995-05">1995-05</date><biblScope unit="vol">10</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="241">241</biblScope><biblScope unit="page" to="249">249</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">9A19ED18260D57A788A678BAC07237BB843FA4EE</idno><idno type="DOI">10.1002/mds.870100302</idno><idno type="ArticleID">MDS870100302</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>6‐[18F]fluoro‐L‐dihydroxyphenylalanine</term><term>Animals</term><term>Brain (physiopathology)</term><term>Brain Mapping</term><term>Corpus Striatum (physiology)</term><term>Dihydroxyphenylalanine (physiology)</term><term>Dopa Decarboxylase (physiology)</term><term>Dopamine (physiology)</term><term>Humans</term><term>L‐Dihydroxyphenylalanine</term><term>L‐Dihydroxyphenylalanine decarboxylase</term><term>Neurotransmitter Agents (physiology)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson's disease</term><term>Positron emission tomography</term><term>Synaptic Transmission (physiology)</term><term>Tomography, Emission-Computed</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dihydroxyphenylalanine</term><term>Dopa Decarboxylase</term><term>Dopamine</term><term>Neurotransmitter Agents</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Corpus Striatum</term><term>Synaptic Transmission</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Brain Mapping</term><term>Humans</term><term>Tomography, Emission-Computed</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Recent experimental reports concerning L‐dihydroxyphenylalanine (L‐DOPA) and aromatic L‐amino acid decarboxylase (AADC, L‐DOPA decarboxylase) are reviewed in this article. Both in vitro and in vivo data now suggest that L‐DOPA is an endogenous neuroactive compound that is released from neurons and acts as a neurotransmitter or neuromodulator in the brain. Administration of exogenous L‐DOPA affects dopamine receptor status, AADC activity, and mitochondrial oxidation in experimental animals. The type and severity of these effects depend on the duration of the treatment. These findings may partly explain the limited efficacy of L‐DOPA therapy in Parkinson's disease (PD). AADC also plays a controlling role in the central nervous system, being a regulatory enzyme in the synthesis of a putative neuromodulator 2‐phenylethylamine and other trace amines. Recent experimental findings on AADC activity and localisation are of importance because they suggest that striatal [18F]DOPA uptake used as an indicator of PD progression in positron emission tomography (PET) studies is likely to overestimate nigrostriatal integrity in advanced PD. Possible new PET tracers of presynaptic dopaminergic function are discussed in this context.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li></region></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Opacka Uffry" sort="Opacka Uffry" uniqKey="Opacka Uffry" last="Opacka-Juffry">Opacka‐Juffry</name></region><name sortKey="Brooks, David J" sort="Brooks, David J" uniqKey="Brooks D" first="David J." last="Brooks">David J. Brooks</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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