Striatal dopamine D1-like receptor binding is unchanged in primary focal dystonia
Identifieur interne : 000066 ( Pmc/Checkpoint ); précédent : 000065; suivant : 000067Striatal dopamine D1-like receptor binding is unchanged in primary focal dystonia
Auteurs : Morvarid Karimi [États-Unis] ; Stephen M. Moerlein [États-Unis] ; Tom O. Videen [États-Unis] ; Y. Su [États-Unis] ; Hubert P. Flores [États-Unis] ; Joel S. Perlmutter [États-Unis]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2013.
Abstract
Multiple studies demonstrate decreases in striatal D2-like (D2, D3) radioligand binding in primary focal dystonias. Although most investigations have focused on D2 specific receptors (D2R), a recent study suggests that the decreased D2-like binding may be due to a D3 specific (D3R) abnormality. However, only limited data exist on the role of D1 specific receptors (D1R) and the D1R-mediated pathways within basal ganglia in dystonia. Metabolic PET data in primary generalized dystonia suggest resting state overactivity in the D1R-mediated "direct" pathway leading to excessive disinhibition of motor cortical areas. This work investigated whether striatal D1-like receptors are affected in primary focal dystonias.
We measured striatal (caudate and putamen) specific binding of the D1-like radioligand [11C] NNC 112 using PET in 19 patients with primary focal dystonia (cranial, cervical or arm) and 18 controls.
We did not detect a statistically significant difference in striatal D1-like binding between the two groups. This study had 91% power to detect a 20% difference, making a false negative study unlikely.
Since [11C] NNC112 has a high affinity for D1-like receptors, very low affinity for D2-like receptors and minimal sensitivity to endogenous dopamine levels, we conclude that D1-like receptor binding is not impaired in these primary focal dystonias.
Url:
DOI: 10.1002/mds.25720
PubMed: 24151192
PubMed Central: 4086787
Affiliations:
- États-Unis
- Missouri (État)
- Saint-Louis (Missouri)
- École de médecine (Université Washington de Saint-Louis)
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<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title>
<p id="P1">Multiple studies demonstrate decreases in striatal D2-like (D2, D3) radioligand binding in primary focal dystonias. Although most investigations have focused on D2 specific receptors (D2R), a recent study suggests that the decreased D2-like binding may be due to a D3 specific (D3R) abnormality. However, only limited data exist on the role of D1 specific receptors (D1R) and the D1R-mediated pathways within basal ganglia in dystonia. Metabolic PET data in primary generalized dystonia suggest resting state overactivity in the D1R-mediated "direct" pathway leading to excessive disinhibition of motor cortical areas. This work investigated whether striatal D1-like receptors are affected in primary focal dystonias.</p>
</sec>
<sec id="S2"><title>Methods</title>
<p id="P2">We measured striatal (caudate and putamen) specific binding of the D1-like radioligand [<sup>11</sup>
C] NNC 112 using PET in 19 patients with primary focal dystonia (cranial, cervical or arm) and 18 controls.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">We did not detect a statistically significant difference in striatal D1-like binding between the two groups. This study had 91% power to detect a 20% difference, making a false negative study unlikely.</p>
</sec>
<sec id="S4"><title>Conclusions</title>
<p id="P4">Since [<sup>11</sup>
C] NNC112 has a high affinity for D1-like receptors, very low affinity for D2-like receptors and minimal sensitivity to endogenous dopamine levels, we conclude that D1-like receptor binding is not impaired in these primary focal dystonias.</p>
</sec>
</div>
</front>
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<journal-id journal-id-type="pubmed-jr-id">5937</journal-id>
<journal-id journal-id-type="nlm-ta">Mov Disord</journal-id>
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<article-id pub-id-type="manuscript">NIHMS531906</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
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<title-group><article-title>Striatal dopamine D1-like receptor binding is unchanged in primary focal dystonia</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Karimi</surname>
<given-names>Morvarid</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Moerlein</surname>
<given-names>Stephen M.</given-names>
</name>
<xref ref-type="aff" rid="A2">2</xref>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Videen</surname>
<given-names>Tom O.</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Su</surname>
<given-names>Y</given-names>
</name>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Flores</surname>
<given-names>Hubert P.</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Perlmutter</surname>
<given-names>Joel S.</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
<xref ref-type="aff" rid="A4">4</xref>
<xref ref-type="aff" rid="A5">5</xref>
<xref ref-type="aff" rid="A6">6</xref>
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<aff id="A1"><label>1</label>
Departments of Neurology, Washington University School of Medicine, Saint Louis, Missouri, USA</aff>
<aff id="A2"><label>2</label>
Mallinckrodt Institute of Radiology, Washington University School of Medicine, Saint Louis, Missouri, USA</aff>
<aff id="A3"><label>3</label>
Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, Saint Louis, Missouri, USA</aff>
<aff id="A4"><label>4</label>
Department of Neurobiology, Washington University School of Medicine, Saint Louis, Missouri, USA</aff>
<aff id="A5"><label>5</label>
Program of Occupational Therapy, Washington University School of Medicine, Saint Louis, Missouri, USA</aff>
<aff id="A6"><label>6</label>
Program of Physical Therapy, Washington University School of Medicine, Saint Louis, Missouri, USA</aff>
<author-notes><corresp id="cor1"><bold>Correspondence:</bold>
M. Karimi, M.D., 660 S. Euclid, Campus Box 8111, St. Louis, MO 63110-1093, Fax: (314) 362-0168, Telephone: (314) 362-6026, <email>morvaridk@npg.wustl.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>29</day>
<month>5</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="epub"><day>21</day>
<month>10</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="ppub"><month>12</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>01</day>
<month>12</month>
<year>2014</year>
</pub-date>
<volume>28</volume>
<issue>14</issue>
<fpage>2002</fpage>
<lpage>2006</lpage>
<pmc-comment>elocation-id from pubmed: 10.1002/mds.25720</pmc-comment>
<abstract><sec id="S1"><title>Background</title>
<p id="P1">Multiple studies demonstrate decreases in striatal D2-like (D2, D3) radioligand binding in primary focal dystonias. Although most investigations have focused on D2 specific receptors (D2R), a recent study suggests that the decreased D2-like binding may be due to a D3 specific (D3R) abnormality. However, only limited data exist on the role of D1 specific receptors (D1R) and the D1R-mediated pathways within basal ganglia in dystonia. Metabolic PET data in primary generalized dystonia suggest resting state overactivity in the D1R-mediated "direct" pathway leading to excessive disinhibition of motor cortical areas. This work investigated whether striatal D1-like receptors are affected in primary focal dystonias.</p>
</sec>
<sec id="S2"><title>Methods</title>
<p id="P2">We measured striatal (caudate and putamen) specific binding of the D1-like radioligand [<sup>11</sup>
C] NNC 112 using PET in 19 patients with primary focal dystonia (cranial, cervical or arm) and 18 controls.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">We did not detect a statistically significant difference in striatal D1-like binding between the two groups. This study had 91% power to detect a 20% difference, making a false negative study unlikely.</p>
</sec>
<sec id="S4"><title>Conclusions</title>
<p id="P4">Since [<sup>11</sup>
C] NNC112 has a high affinity for D1-like receptors, very low affinity for D2-like receptors and minimal sensitivity to endogenous dopamine levels, we conclude that D1-like receptor binding is not impaired in these primary focal dystonias.</p>
</sec>
</abstract>
<kwd-group><kwd>PET</kwd>
<kwd>focal dystonia</kwd>
<kwd>D1 receptor</kwd>
<kwd>[<sup>11</sup>
C] NNC 112</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Missouri (État)</li>
</region>
<settlement><li>Saint-Louis (Missouri)</li>
</settlement>
<orgName><li>École de médecine (Université Washington de Saint-Louis)</li>
</orgName>
</list>
<tree><country name="États-Unis"><region name="Missouri (État)"><name sortKey="Karimi, Morvarid" sort="Karimi, Morvarid" uniqKey="Karimi M" first="Morvarid" last="Karimi">Morvarid Karimi</name>
</region>
<name sortKey="Flores, Hubert P" sort="Flores, Hubert P" uniqKey="Flores H" first="Hubert P." last="Flores">Hubert P. Flores</name>
<name sortKey="Moerlein, Stephen M" sort="Moerlein, Stephen M" uniqKey="Moerlein S" first="Stephen M." last="Moerlein">Stephen M. Moerlein</name>
<name sortKey="Moerlein, Stephen M" sort="Moerlein, Stephen M" uniqKey="Moerlein S" first="Stephen M." last="Moerlein">Stephen M. Moerlein</name>
<name sortKey="Perlmutter, Joel S" sort="Perlmutter, Joel S" uniqKey="Perlmutter J" first="Joel S." last="Perlmutter">Joel S. Perlmutter</name>
<name sortKey="Perlmutter, Joel S" sort="Perlmutter, Joel S" uniqKey="Perlmutter J" first="Joel S." last="Perlmutter">Joel S. Perlmutter</name>
<name sortKey="Perlmutter, Joel S" sort="Perlmutter, Joel S" uniqKey="Perlmutter J" first="Joel S." last="Perlmutter">Joel S. Perlmutter</name>
<name sortKey="Perlmutter, Joel S" sort="Perlmutter, Joel S" uniqKey="Perlmutter J" first="Joel S." last="Perlmutter">Joel S. Perlmutter</name>
<name sortKey="Perlmutter, Joel S" sort="Perlmutter, Joel S" uniqKey="Perlmutter J" first="Joel S." last="Perlmutter">Joel S. Perlmutter</name>
<name sortKey="Su, Y" sort="Su, Y" uniqKey="Su Y" first="Y" last="Su">Y. Su</name>
<name sortKey="Videen, Tom O" sort="Videen, Tom O" uniqKey="Videen T" first="Tom O." last="Videen">Tom O. Videen</name>
<name sortKey="Videen, Tom O" sort="Videen, Tom O" uniqKey="Videen T" first="Tom O." last="Videen">Tom O. Videen</name>
</country>
</tree>
</affiliations>
</record>
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