Brain Interstitial Nociceptin/Orphanin FQ Levels are Elevated in Parkinson's Disease
Identifieur interne : 000793 ( Main/Exploration ); précédent : 000792; suivant : 000794Brain Interstitial Nociceptin/Orphanin FQ Levels are Elevated in Parkinson's Disease
Auteurs : Matteo Marti [Italie] ; Silvio Sarubbo [Italie] ; Francesco Latini [Italie] ; Michele Cavallo [Italie] ; Roberto Eleopra [Italie] ; Sara Biguzzi [Italie] ; Christian Lettieri [Italie] ; Carlo Conti [Italie] ; Michele Simonato [Italie] ; Silvia Zucchini [Italie] ; Rocco Quatrale [Italie] ; Mariachiara Sensi [Italie] ; Sanzio Candeletti [Italie] ; Patrizia Romualdi [Italie] ; Michele Morari [Italie]Source :
- Movement Disorders [ 0885-3185 ] ; 2010-08-15.
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Abstract
Expression and release of nociceptin/orphanin FQ (N/OFQ) are elevated in the substantia nigra reticulata of 6‐hydroxydopamine‐hemilesioned rats, suggesting a pathogenic role for N/OFQ in Parkinson's disease. In this study, we investigated whether elevation of N/OFQ expression in 6‐hydroxydopamine‐hemilesioned rats selectively occurs in substantia nigra and whether hypomotility following acute haloperidol administration is accompanied by a rise in nigral N/OFQ levels. Moreover, to prove a link between N/OFQ and idiopathic Parkinson's disease in humans, we measured N/OFQ levels in the cerebrospinal fluid of parkinsonian patients undergoing surgery for deep brain stimulation. In situ hybridization demonstrated that dopamine depletion was associated with increase of N/OFQ expression in substantia nigra (compacta +160%, reticulata +105%) and subthalamic nucleus (+45%), as well as reduction in caudate putamen (−20%). No change was observed in globus pallidus, nucleus accumbens, thalamus, and motor cortex. Microdialysis coupled to the bar test allowed to demonstrate that acute administration of haloperidol (0.8 and 3 mg/kg) increased nigral N/OFQ levels (maximally of +47% and +53%, respectively) in parallel with akinesia. A correlation with preclinical studies was found by analyzing N/OFQ levels in humans. Indeed, N/OFQ levels were found to be ∼3.5‐fold elevated in the cerebrospinal fluid of parkinsonian patients (148 fmol/ml) compared with nonparkinsonian neurologic controls (41 fmol/ml). These data represent the first clinical evidence linking N/OFQ to idiopathic Parkinson's disease in humans. They strengthen the pathogenic role of N/OFQ in the modulation of parkinsonism across species and provide a rationale for developing N/OFQ receptor antagonists as antiparkinsonian drugs. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23271
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Anna University Hospital of Ferrara, Ferrara</wicri:regionArea><wicri:noRegion>Ferrara</wicri:noRegion></affiliation></author><author><name sortKey="Candeletti, Sanzio" sort="Candeletti, Sanzio" uniqKey="Candeletti S" first="Sanzio" last="Candeletti">Sanzio Candeletti</name><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Pharmacology, University of Bologna, Bologna</wicri:regionArea><wicri:noRegion>Bologna</wicri:noRegion></affiliation></author><author><name sortKey="Romualdi, Patrizia" sort="Romualdi, Patrizia" uniqKey="Romualdi P" first="Patrizia" last="Romualdi">Patrizia Romualdi</name><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Pharmacology, University of Bologna, Bologna</wicri:regionArea><wicri:noRegion>Bologna</wicri:noRegion></affiliation></author><author><name sortKey="Morari, Michele" sort="Morari, Michele" uniqKey="Morari M" first="Michele" last="Morari">Michele Morari</name><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Experimental and Clinical Medicine, Section of Pharmacology, University of Ferrara, Ferrara</wicri:regionArea><wicri:noRegion>Ferrara</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Center for Neuroscience and National Institute of Neuroscience, University of Ferrara, Ferrara</wicri:regionArea><wicri:noRegion>Ferrara</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</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="2010-08-15">2010-08-15</date><biblScope unit="volume">25</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="1723">1723</biblScope><biblScope unit="page" to="1732">1732</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">1CE9DF3823E287CFB399BE284462445B5293F1E5</idno><idno type="DOI">10.1002/mds.23271</idno><idno type="ArticleID">MDS23271</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>6‐OHDA</term><term>Parkinson's disease</term><term>cerebrospinal fluid</term><term>haloperidol</term><term>human</term><term>nociceptin/orphanin FQ</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Expression and release of nociceptin/orphanin FQ (N/OFQ) are elevated in the substantia nigra reticulata of 6‐hydroxydopamine‐hemilesioned rats, suggesting a pathogenic role for N/OFQ in Parkinson's disease. In this study, we investigated whether elevation of N/OFQ expression in 6‐hydroxydopamine‐hemilesioned rats selectively occurs in substantia nigra and whether hypomotility following acute haloperidol administration is accompanied by a rise in nigral N/OFQ levels. Moreover, to prove a link between N/OFQ and idiopathic Parkinson's disease in humans, we measured N/OFQ levels in the cerebrospinal fluid of parkinsonian patients undergoing surgery for deep brain stimulation. In situ hybridization demonstrated that dopamine depletion was associated with increase of N/OFQ expression in substantia nigra (compacta +160%, reticulata +105%) and subthalamic nucleus (+45%), as well as reduction in caudate putamen (−20%). No change was observed in globus pallidus, nucleus accumbens, thalamus, and motor cortex. Microdialysis coupled to the bar test allowed to demonstrate that acute administration of haloperidol (0.8 and 3 mg/kg) increased nigral N/OFQ levels (maximally of +47% and +53%, respectively) in parallel with akinesia. A correlation with preclinical studies was found by analyzing N/OFQ levels in humans. Indeed, N/OFQ levels were found to be ∼3.5‐fold elevated in the cerebrospinal fluid of parkinsonian patients (148 fmol/ml) compared with nonparkinsonian neurologic controls (41 fmol/ml). These data represent the first clinical evidence linking N/OFQ to idiopathic Parkinson's disease in humans. They strengthen the pathogenic role of N/OFQ in the modulation of parkinsonism across species and provide a rationale for developing N/OFQ receptor antagonists as antiparkinsonian drugs. © 2010 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Italie</li></country></list><tree><country name="Italie"><noRegion><name sortKey="Marti, Matteo" sort="Marti, Matteo" uniqKey="Marti M" first="Matteo" last="Marti">Matteo Marti</name></noRegion><name sortKey="Biguzzi, Sara" sort="Biguzzi, Sara" uniqKey="Biguzzi S" first="Sara" last="Biguzzi">Sara Biguzzi</name><name sortKey="Candeletti, Sanzio" sort="Candeletti, Sanzio" uniqKey="Candeletti S" first="Sanzio" last="Candeletti">Sanzio Candeletti</name><name sortKey="Cavallo, Michele" sort="Cavallo, Michele" uniqKey="Cavallo M" first="Michele" last="Cavallo">Michele Cavallo</name><name sortKey="Conti, Carlo" sort="Conti, Carlo" uniqKey="Conti C" first="Carlo" last="Conti">Carlo Conti</name><name sortKey="Eleopra, Roberto" sort="Eleopra, Roberto" uniqKey="Eleopra R" first="Roberto" last="Eleopra">Roberto Eleopra</name><name sortKey="Latini, Francesco" sort="Latini, Francesco" uniqKey="Latini F" first="Francesco" last="Latini">Francesco Latini</name><name sortKey="Lettieri, Christian" sort="Lettieri, Christian" uniqKey="Lettieri C" first="Christian" last="Lettieri">Christian Lettieri</name><name sortKey="Marti, Matteo" sort="Marti, Matteo" uniqKey="Marti M" first="Matteo" last="Marti">Matteo Marti</name><name sortKey="Morari, Michele" sort="Morari, Michele" uniqKey="Morari M" first="Michele" last="Morari">Michele Morari</name><name sortKey="Morari, Michele" sort="Morari, Michele" uniqKey="Morari M" first="Michele" last="Morari">Michele Morari</name><name sortKey="Quatrale, Rocco" sort="Quatrale, Rocco" uniqKey="Quatrale R" first="Rocco" last="Quatrale">Rocco Quatrale</name><name sortKey="Romualdi, Patrizia" sort="Romualdi, Patrizia" uniqKey="Romualdi P" first="Patrizia" last="Romualdi">Patrizia Romualdi</name><name sortKey="Sarubbo, Silvio" sort="Sarubbo, Silvio" uniqKey="Sarubbo S" first="Silvio" last="Sarubbo">Silvio Sarubbo</name><name sortKey="Sensi, Mariachiara" sort="Sensi, Mariachiara" uniqKey="Sensi M" first="Mariachiara" last="Sensi">Mariachiara Sensi</name><name sortKey="Simonato, Michele" sort="Simonato, Michele" uniqKey="Simonato M" first="Michele" last="Simonato">Michele Simonato</name><name sortKey="Simonato, Michele" sort="Simonato, Michele" uniqKey="Simonato M" first="Michele" last="Simonato">Michele Simonato</name><name sortKey="Zucchini, Silvia" sort="Zucchini, Silvia" uniqKey="Zucchini S" first="Silvia" last="Zucchini">Silvia Zucchini</name><name sortKey="Zucchini, Silvia" sort="Zucchini, Silvia" uniqKey="Zucchini S" first="Silvia" last="Zucchini">Silvia Zucchini</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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