Dysregulation of striatal dopamine release in a mouse model of dystonia
Identifieur interne : 000293 ( Ncbi/Merge ); précédent : 000292; suivant : 000294Dysregulation of striatal dopamine release in a mouse model of dystonia
Auteurs : Li Bao [États-Unis] ; Jyoti Patel [États-Unis] ; Ruth Walker [États-Unis] ; Pullanipally Shashidharan [États-Unis] ; Margaret Rice [États-Unis]Source :
- Journal of neurochemistry [ 0022-3042 ] ; 2010.
Abstract
Dystonia is a neurological disorder characterized by involuntary movements. We examined striatal dopamine function in hyperactive transgenic mice generated as a model of dystonia. Evoked extracellular dopamine concentration was monitored with carbon-fiber microelectrodes and fast-scan cyclic voltammetry in striatal slices from non-transgenic mice, transgenic mice with a positive motor phenotype, and phenotype-negative transgenic littermates. Peak single-pulse evoked dopamine concentration was significantly lower in phenotype-positive mice than in non-transgenic or phenotype-negative mice, but indistinguishable between non-transgenic and phenotype-negative mice. Phenotype-positive mice also had higher functional D2 dopamine autoreceptor sensitivity than non-transgenic mice, which would be consistent with lower extracellular dopamine concentration
Url:
DOI: 10.1111/j.1471-4159.2010.06890.x
PubMed: 20626557
PubMed Central: 2951331
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<front><div type="abstract" xml:lang="en"><p id="P2">Dystonia is a neurological disorder characterized by involuntary movements. We examined striatal dopamine function in hyperactive transgenic mice generated as a model of dystonia. Evoked extracellular dopamine concentration was monitored with carbon-fiber microelectrodes and fast-scan cyclic voltammetry in striatal slices from non-transgenic mice, transgenic mice with a positive motor phenotype, and phenotype-negative transgenic littermates. Peak single-pulse evoked dopamine concentration was significantly lower in phenotype-positive mice than in non-transgenic or phenotype-negative mice, but indistinguishable between non-transgenic and phenotype-negative mice. Phenotype-positive mice also had higher functional D2 dopamine autoreceptor sensitivity than non-transgenic mice, which would be consistent with lower extracellular dopamine concentration <italic>in vivo</italic>
. Multiple-pulse (phasic) stimulation (5 pulses, 10-100 Hz) revealed an enhanced frequency dependence of evoked dopamine release in phenotype-positive <italic>versus</italic>
non-transgenic or phenotype-negative mice, which was exacerbated when extracellular Ca<sup>2+</sup>
concentration was lowered. Enhanced sensitivity to phasic stimulation in phenotype-positive mice was reminiscent of the pattern seen with antagonism of nicotinic acetylcholine receptors. Consistent with a role for altered cholinergic regulation, the difference in phasic responsiveness among groups was lost when nicotinic receptors were blocked by mecamylamine. Together, these data implicate compromised dopamine release regulation, possibly from cholinergic dysfunction, in the motor symptoms of this dystonia model.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article" xml:lang="EN"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
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<front><journal-meta><journal-id journal-id-type="nlm-journal-id">2985190R</journal-id>
<journal-id journal-id-type="pubmed-jr-id">5004</journal-id>
<journal-id journal-id-type="nlm-ta">J Neurochem</journal-id>
<journal-title>Journal of neurochemistry</journal-title>
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<issn pub-type="epub">1471-4159</issn>
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<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Dysregulation of striatal dopamine release in a mouse model of dystonia</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Bao</surname>
<given-names>Li</given-names>
</name>
<xref ref-type="author-notes" rid="FN1">*</xref>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Patel</surname>
<given-names>Jyoti C.</given-names>
</name>
<xref ref-type="author-notes" rid="FN1">*</xref>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Walker</surname>
<given-names>Ruth H.</given-names>
</name>
<xref ref-type="aff" rid="A3">3</xref>
<xref ref-type="aff" rid="A4">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Shashidharan</surname>
<given-names>Pullanipally</given-names>
</name>
<xref ref-type="aff" rid="A4">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Rice</surname>
<given-names>Margaret E.</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>1</label>
Department of Physiology and Neuroscience NYU School of Medicine, New York, NY USA</aff>
<aff id="A2"><label>2</label>
Department of Neurosurgery NYU School of Medicine, New York, NY USA</aff>
<aff id="A3"><label>3</label>
Department of Neurology, James J. Peters Veterans Affairs Medical Center, Bronx, NY USA</aff>
<aff id="A4"><label>4</label>
Department of Neurology, Mount Sinai School of Medicine, New York, NY USA</aff>
<author-notes><corresp id="CR1"><bold>Correspondence to:</bold>
Dr. Margaret E. Rice, Dept. Physiology and Neuroscience, NYU School of Medicine, 550 First Avenue, New York, NY, 10016, <bold>Telephone:</bold>
212-263-5438, <bold>Fax:</bold>
212-689-0334, <email>margaret.rice@nyu.edu</email>
</corresp>
<fn fn-type="equal" id="FN1"><label>*</label>
<p id="P1">These authors contributed equally to this study</p>
</fn>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>9</day>
<month>8</month>
<year>2010</year>
</pub-date>
<pub-date pub-type="epub"><day>27</day>
<month>7</month>
<year>2010</year>
</pub-date>
<pub-date pub-type="ppub"><month>9</month>
<year>2010</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>1</day>
<month>9</month>
<year>2011</year>
</pub-date>
<volume>114</volume>
<issue>6</issue>
<fpage>1781</fpage>
<lpage>1791</lpage>
<abstract><p id="P2">Dystonia is a neurological disorder characterized by involuntary movements. We examined striatal dopamine function in hyperactive transgenic mice generated as a model of dystonia. Evoked extracellular dopamine concentration was monitored with carbon-fiber microelectrodes and fast-scan cyclic voltammetry in striatal slices from non-transgenic mice, transgenic mice with a positive motor phenotype, and phenotype-negative transgenic littermates. Peak single-pulse evoked dopamine concentration was significantly lower in phenotype-positive mice than in non-transgenic or phenotype-negative mice, but indistinguishable between non-transgenic and phenotype-negative mice. Phenotype-positive mice also had higher functional D2 dopamine autoreceptor sensitivity than non-transgenic mice, which would be consistent with lower extracellular dopamine concentration <italic>in vivo</italic>
. Multiple-pulse (phasic) stimulation (5 pulses, 10-100 Hz) revealed an enhanced frequency dependence of evoked dopamine release in phenotype-positive <italic>versus</italic>
non-transgenic or phenotype-negative mice, which was exacerbated when extracellular Ca<sup>2+</sup>
concentration was lowered. Enhanced sensitivity to phasic stimulation in phenotype-positive mice was reminiscent of the pattern seen with antagonism of nicotinic acetylcholine receptors. Consistent with a role for altered cholinergic regulation, the difference in phasic responsiveness among groups was lost when nicotinic receptors were blocked by mecamylamine. Together, these data implicate compromised dopamine release regulation, possibly from cholinergic dysfunction, in the motor symptoms of this dystonia model.</p>
</abstract>
<kwd-group><kwd>Acetylcholine</kwd>
<kwd>ACh</kwd>
<kwd>basal ganglia</kwd>
<kwd>brain slices</kwd>
<kwd>early-onset dystonia</kwd>
<kwd>voltammetry</kwd>
</kwd-group>
<contract-num rid="NS1">R01 NS043038-08
||NS</contract-num>
<contract-num rid="NS1">R01 NS036362-12
||NS</contract-num>
<contract-sponsor id="NS1">National Institute of Neurological Disorders and Stroke : NINDS</contract-sponsor>
</article-meta>
</front>
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