Anticholinergic drugs rescue synaptic plasticity in DYT1 dystonia: role of M1 muscarinic receptors.
Identifieur interne : 000397 ( PubMed/Corpus ); précédent : 000396; suivant : 000398Anticholinergic drugs rescue synaptic plasticity in DYT1 dystonia: role of M1 muscarinic receptors.
Auteurs : Marta Maltese ; Giuseppina Martella ; Graziella Madeo ; Irene Fagiolo ; Annalisa Tassone ; Giulia Ponterio ; Giuseppe Sciamanna ; Pierre Burbaud ; P Jeffrey Conn ; Paola Bonsi ; Antonio PisaniSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Biophysics, Cholinergic Antagonists (pharmacology), Corpus Striatum (cytology), Electric Stimulation, Excitatory Postsynaptic Potentials (drug effects), In Vitro Techniques, Long-Term Potentiation (drug effects), Mice, Mice, Transgenic, Molecular Chaperones (genetics), Mutation (genetics), Neurons (drug effects), Patch-Clamp Techniques, Synapses (drug effects), Synapses (genetics), Thalamus (cytology).
- MESH :
- chemical , genetics : Molecular Chaperones.
- chemical , pharmacology : Cholinergic Antagonists.
- cytology : Corpus Striatum, Thalamus.
- drug effects : Excitatory Postsynaptic Potentials, Long-Term Potentiation, Neurons, Synapses.
- genetics : Mutation, Synapses.
- Animals, Biophysics, Electric Stimulation, In Vitro Techniques, Mice, Mice, Transgenic, Patch-Clamp Techniques.
Abstract
Broad-spectrum muscarinic receptor antagonists have represented the first available treatment for different movement disorders such as dystonia. However, the specificity of these drugs and their mechanism of action is not entirely clear. We performed a systematic analysis of the effects of anticholinergic drugs on short- and long-term plasticity recorded from striatal medium spiny neurons from DYT1 dystonia knock-in (Tor1a(+/Δgag) ) mice heterozygous for ΔE-torsinA and their controls (Tor1a(+/+) mice). Antagonists were chosen that had previously been proposed to be selective for muscarinic receptor subtypes and included pirenzepine, trihexyphenydil, biperiden, orphenadrine, and a novel selective M1 antagonist, VU0255035. Tor1a(+/Δgag) mice exhibited a significant impairment of corticostriatal synaptic plasticity. Anticholinergics had no significant effects on intrinsic membrane properties and on short-term plasticity of striatal neurons. However, they exhibited a differential ability to restore the corticostriatal plasticity deficits. A complete rescue of both long-term depression (LTD) and synaptic depotentiation (SD) was obtained by applying the M1 -preferring antagonists pirenzepine and trihexyphenidyl as well as VU0255035. Conversely, the nonselective antagonist orphenadrine produced only a partial rescue of synaptic plasticity, whereas biperiden and ethopropazine failed to restore plasticity. The selectivity for M1 receptors was further demonstrated by their ability to counteract the M1 -dependent potentiation of N-methyl-d-aspartate (NMDA) current recorded from striatal neurons. Our study demonstrates that selective M1 muscarinic receptor antagonism offsets synaptic plasticity deficits in the striatum of mice with the DYT1 dystonia mutation, providing a potential mechanistic rationale for the development of improved antimuscarinic therapies for this movement disorder.
DOI: 10.1002/mds.26009
PubMed: 25195914
Links to Exploration step
pubmed:25195914Le document en format XML
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IRCCS Fondazione Santa Lucia, Rome, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Martella, Giuseppina" sort="Martella, Giuseppina" uniqKey="Martella G" first="Giuseppina" last="Martella">Giuseppina Martella</name></author><author><name sortKey="Madeo, Graziella" sort="Madeo, Graziella" uniqKey="Madeo G" first="Graziella" last="Madeo">Graziella Madeo</name></author><author><name sortKey="Fagiolo, Irene" sort="Fagiolo, Irene" uniqKey="Fagiolo I" first="Irene" last="Fagiolo">Irene Fagiolo</name></author><author><name sortKey="Tassone, Annalisa" sort="Tassone, Annalisa" uniqKey="Tassone A" first="Annalisa" last="Tassone">Annalisa Tassone</name></author><author><name sortKey="Ponterio, Giulia" sort="Ponterio, Giulia" uniqKey="Ponterio G" first="Giulia" last="Ponterio">Giulia Ponterio</name></author><author><name sortKey="Sciamanna, Giuseppe" sort="Sciamanna, Giuseppe" uniqKey="Sciamanna G" first="Giuseppe" last="Sciamanna">Giuseppe Sciamanna</name></author><author><name sortKey="Burbaud, Pierre" sort="Burbaud, Pierre" uniqKey="Burbaud P" first="Pierre" last="Burbaud">Pierre Burbaud</name></author><author><name sortKey="Conn, P Jeffrey" sort="Conn, P Jeffrey" uniqKey="Conn P" first="P Jeffrey" last="Conn">P Jeffrey Conn</name></author><author><name sortKey="Bonsi, Paola" sort="Bonsi, Paola" uniqKey="Bonsi P" first="Paola" last="Bonsi">Paola Bonsi</name></author><author><name sortKey="Pisani, Antonio" sort="Pisani, Antonio" uniqKey="Pisani A" first="Antonio" last="Pisani">Antonio Pisani</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Biophysics</term><term>Cholinergic Antagonists (pharmacology)</term><term>Corpus Striatum (cytology)</term><term>Electric Stimulation</term><term>Excitatory Postsynaptic Potentials (drug effects)</term><term>In Vitro Techniques</term><term>Long-Term Potentiation (drug effects)</term><term>Mice</term><term>Mice, Transgenic</term><term>Molecular Chaperones (genetics)</term><term>Mutation (genetics)</term><term>Neurons (drug effects)</term><term>Patch-Clamp Techniques</term><term>Synapses (drug effects)</term><term>Synapses (genetics)</term><term>Thalamus (cytology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Molecular Chaperones</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Cholinergic Antagonists</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Corpus Striatum</term><term>Thalamus</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Excitatory Postsynaptic Potentials</term><term>Long-Term Potentiation</term><term>Neurons</term><term>Synapses</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term><term>Synapses</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Biophysics</term><term>Electric Stimulation</term><term>In Vitro Techniques</term><term>Mice</term><term>Mice, Transgenic</term><term>Patch-Clamp Techniques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Broad-spectrum muscarinic receptor antagonists have represented the first available treatment for different movement disorders such as dystonia. However, the specificity of these drugs and their mechanism of action is not entirely clear. We performed a systematic analysis of the effects of anticholinergic drugs on short- and long-term plasticity recorded from striatal medium spiny neurons from DYT1 dystonia knock-in (Tor1a(+/Δgag) ) mice heterozygous for ΔE-torsinA and their controls (Tor1a(+/+) mice). Antagonists were chosen that had previously been proposed to be selective for muscarinic receptor subtypes and included pirenzepine, trihexyphenydil, biperiden, orphenadrine, and a novel selective M1 antagonist, VU0255035. Tor1a(+/Δgag) mice exhibited a significant impairment of corticostriatal synaptic plasticity. Anticholinergics had no significant effects on intrinsic membrane properties and on short-term plasticity of striatal neurons. However, they exhibited a differential ability to restore the corticostriatal plasticity deficits. A complete rescue of both long-term depression (LTD) and synaptic depotentiation (SD) was obtained by applying the M1 -preferring antagonists pirenzepine and trihexyphenidyl as well as VU0255035. Conversely, the nonselective antagonist orphenadrine produced only a partial rescue of synaptic plasticity, whereas biperiden and ethopropazine failed to restore plasticity. The selectivity for M1 receptors was further demonstrated by their ability to counteract the M1 -dependent potentiation of N-methyl-d-aspartate (NMDA) current recorded from striatal neurons. Our study demonstrates that selective M1 muscarinic receptor antagonism offsets synaptic plasticity deficits in the striatum of mice with the DYT1 dystonia mutation, providing a potential mechanistic rationale for the development of improved antimuscarinic therapies for this movement disorder.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">25195914</PMID><DateCreated><Year>2014</Year><Month>11</Month><Day>01</Day></DateCreated><DateCompleted><Year>2015</Year><Month>06</Month><Day>22</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>29</Volume><Issue>13</Issue><PubDate><Year>2014</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Anticholinergic drugs rescue synaptic plasticity in DYT1 dystonia: role of M1 muscarinic receptors.</ArticleTitle><Pagination><MedlinePgn>1655-65</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.26009</ELocationID><Abstract><AbstractText>Broad-spectrum muscarinic receptor antagonists have represented the first available treatment for different movement disorders such as dystonia. However, the specificity of these drugs and their mechanism of action is not entirely clear. We performed a systematic analysis of the effects of anticholinergic drugs on short- and long-term plasticity recorded from striatal medium spiny neurons from DYT1 dystonia knock-in (Tor1a(+/Δgag) ) mice heterozygous for ΔE-torsinA and their controls (Tor1a(+/+) mice). Antagonists were chosen that had previously been proposed to be selective for muscarinic receptor subtypes and included pirenzepine, trihexyphenydil, biperiden, orphenadrine, and a novel selective M1 antagonist, VU0255035. Tor1a(+/Δgag) mice exhibited a significant impairment of corticostriatal synaptic plasticity. Anticholinergics had no significant effects on intrinsic membrane properties and on short-term plasticity of striatal neurons. However, they exhibited a differential ability to restore the corticostriatal plasticity deficits. A complete rescue of both long-term depression (LTD) and synaptic depotentiation (SD) was obtained by applying the M1 -preferring antagonists pirenzepine and trihexyphenidyl as well as VU0255035. Conversely, the nonselective antagonist orphenadrine produced only a partial rescue of synaptic plasticity, whereas biperiden and ethopropazine failed to restore plasticity. The selectivity for M1 receptors was further demonstrated by their ability to counteract the M1 -dependent potentiation of N-methyl-d-aspartate (NMDA) current recorded from striatal neurons. Our study demonstrates that selective M1 muscarinic receptor antagonism offsets synaptic plasticity deficits in the striatum of mice with the DYT1 dystonia mutation, providing a potential mechanistic rationale for the development of improved antimuscarinic therapies for this movement disorder.</AbstractText><CopyrightInformation>© 2014 International Parkinson and Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Maltese</LastName><ForeName>Marta</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Systems Medicine, University of Rome "Tor Vergata", Italy; IRCCS Fondazione Santa Lucia, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martella</LastName><ForeName>Giuseppina</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Madeo</LastName><ForeName>Graziella</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Fagiolo</LastName><ForeName>Irene</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Tassone</LastName><ForeName>Annalisa</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Ponterio</LastName><ForeName>Giulia</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Sciamanna</LastName><ForeName>Giuseppe</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Burbaud</LastName><ForeName>Pierre</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Conn</LastName><ForeName>P Jeffrey</ForeName><Initials>PJ</Initials></Author><Author ValidYN="Y"><LastName>Bonsi</LastName><ForeName>Paola</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Pisani</LastName><ForeName>Antonio</ForeName><Initials>A</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 MH073676</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS065867</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U01 MH087965</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>09</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018680">Cholinergic Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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PubStatus="received"><Year>2014</Year><Month>7</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>8</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>8</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2014</Year><Month>9</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>9</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>9</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>6</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25195914</ArticleId><ArticleId IdType="doi">10.1002/mds.26009</ArticleId><ArticleId IdType="pmc">PMC4216601</ArticleId><ArticleId 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