Mutant LRRK2 enhances glutamatergic synapse activity and evokes excitotoxic dendrite degeneration.
Identifieur interne : 001E52 ( PubMed/Corpus ); précédent : 001E51; suivant : 001E53Mutant LRRK2 enhances glutamatergic synapse activity and evokes excitotoxic dendrite degeneration.
Auteurs : Edward D. Plowey ; Jon W. Johnson ; Erin Steer ; Wan Zhu ; David A. Eisenberg ; Natalie M. Valentino ; Yong-Jian Liu ; Charleen T. ChuSource :
- Biochimica et biophysica acta [ 0006-3002 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Calcium (metabolism), Cells, Cultured, Dendrites (drug effects), Dendrites (physiology), Dopamine Agents (pharmacology), Electrophysiology, Female, Glutamates (metabolism), Immunoenzyme Techniques, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Memantine (pharmacology), Mutation (genetics), Neurons (drug effects), Neurons (physiology), Protein-Serine-Threonine Kinases (genetics), Protein-Serine-Threonine Kinases (metabolism), Rats, Rats, Sprague-Dawley, Signal Transduction (drug effects), Synapses (drug effects), Synapses (physiology), Synaptosomes (physiology).
- MESH :
- chemical , genetics : Protein-Serine-Threonine Kinases.
- chemical , metabolism : Calcium, Glutamates, Protein-Serine-Threonine Kinases.
- drug effects : Dendrites, Neurons, Signal Transduction, Synapses.
- genetics : Mutation.
- chemical , pharmacology : Dopamine Agents, Memantine.
- physiology : Dendrites, Neurons, Synapses, Synaptosomes.
- Animals, Cells, Cultured, Electrophysiology, Female, Immunoenzyme Techniques, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Rats, Rats, Sprague-Dawley.
Abstract
Mutations in leucine-rich repeat kinase 2 (LRRK2), which are associated with autosomal dominant Parkinson's disease, elicit progressive dendrite degeneration in neurons. We hypothesized that synaptic dysregulation contributes to mutant LRRK2-induced dendritic injury. We performed in vitro whole-cell voltage clamp studies of glutamatergic receptor agonist responses and glutamatergic synaptic activity in cultured rat cortical neurons expressing full-length wild-type and mutant forms of LRRK2. Expression of the pathogenic G2019S or R1441C LRRK2 mutants resulted in larger whole-cell current responses to direct application of AMPA and NMDA receptor agonists. In addition, mutant LRRK2-expressing neurons exhibited an increased frequency of spontaneous miniature excitatory postsynaptic currents (mEPSCs) in conjunction with increased excitatory synapse density as assessed by immunofluorescence for PSD95 and VGLUT1. Mutant LRRK2-expressing neurons showed enhanced vulnerability to acute synaptic glutamate stress. Furthermore, treatment with the NMDA receptor antagonist memantine significantly protected against subsequent losses in dendrite length and branching complexity. These data demonstrate an early association between mutant LRRK2 and increased excitatory synapse activity, implicating an excitotoxic contribution to mutant LRRK2 induced dendrite degeneration.
DOI: 10.1016/j.bbadis.2014.05.016
PubMed: 24874075
Links to Exploration step
pubmed:24874075Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mutant LRRK2 enhances glutamatergic synapse activity and evokes excitotoxic dendrite degeneration.</title><author><name sortKey="Plowey, Edward D" sort="Plowey, Edward D" uniqKey="Plowey E" first="Edward D" last="Plowey">Edward D. Plowey</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Pathology, Stanford University, Stanford, CA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Johnson, Jon W" sort="Johnson, Jon W" uniqKey="Johnson J" first="Jon W" last="Johnson">Jon W. Johnson</name><affiliation><nlm:affiliation>Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA; Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA; The Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Steer, Erin" sort="Steer, Erin" uniqKey="Steer E" first="Erin" last="Steer">Erin Steer</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Zhu, Wan" sort="Zhu, Wan" uniqKey="Zhu W" first="Wan" last="Zhu">Wan Zhu</name><affiliation><nlm:affiliation>Department of Pathology, Stanford University, Stanford, CA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Eisenberg, David A" sort="Eisenberg, David A" uniqKey="Eisenberg D" first="David A" last="Eisenberg">David A. Eisenberg</name><affiliation><nlm:affiliation>Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Valentino, Natalie M" sort="Valentino, Natalie M" uniqKey="Valentino N" first="Natalie M" last="Valentino">Natalie M. Valentino</name><affiliation><nlm:affiliation>Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Yong Jian" sort="Liu, Yong Jian" uniqKey="Liu Y" first="Yong-Jian" last="Liu">Yong-Jian Liu</name><affiliation><nlm:affiliation>Department of Physiology, Nanjing Medical University, Nanjing, China.</nlm:affiliation></affiliation></author><author><name sortKey="Chu, Charleen T" sort="Chu, Charleen T" uniqKey="Chu C" first="Charleen T" last="Chu">Charleen T. Chu</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Ophthalmology, University of Pittsburgh, Pittsburgh, PA, USA; The McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, USA; The Pittsburgh Institute for Neurodegenerative Diseases, University of Pittsburgh, Pittsburgh, PA, USA; The Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA. Electronic address: ctc4@pitt.edu.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24874075</idno><idno type="pmid">24874075</idno><idno type="doi">10.1016/j.bbadis.2014.05.016</idno><idno type="wicri:Area/PubMed/Corpus">001E52</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001E52</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Mutant LRRK2 enhances glutamatergic synapse activity and evokes excitotoxic dendrite degeneration.</title><author><name sortKey="Plowey, Edward D" sort="Plowey, Edward D" uniqKey="Plowey E" first="Edward D" last="Plowey">Edward D. Plowey</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Pathology, Stanford University, Stanford, CA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Johnson, Jon W" sort="Johnson, Jon W" uniqKey="Johnson J" first="Jon W" last="Johnson">Jon W. Johnson</name><affiliation><nlm:affiliation>Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA; Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA; The Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Steer, Erin" sort="Steer, Erin" uniqKey="Steer E" first="Erin" last="Steer">Erin Steer</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Zhu, Wan" sort="Zhu, Wan" uniqKey="Zhu W" first="Wan" last="Zhu">Wan Zhu</name><affiliation><nlm:affiliation>Department of Pathology, Stanford University, Stanford, CA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Eisenberg, David A" sort="Eisenberg, David A" uniqKey="Eisenberg D" first="David A" last="Eisenberg">David A. Eisenberg</name><affiliation><nlm:affiliation>Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Valentino, Natalie M" sort="Valentino, Natalie M" uniqKey="Valentino N" first="Natalie M" last="Valentino">Natalie M. Valentino</name><affiliation><nlm:affiliation>Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Yong Jian" sort="Liu, Yong Jian" uniqKey="Liu Y" first="Yong-Jian" last="Liu">Yong-Jian Liu</name><affiliation><nlm:affiliation>Department of Physiology, Nanjing Medical University, Nanjing, China.</nlm:affiliation></affiliation></author><author><name sortKey="Chu, Charleen T" sort="Chu, Charleen T" uniqKey="Chu C" first="Charleen T" last="Chu">Charleen T. Chu</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Ophthalmology, University of Pittsburgh, Pittsburgh, PA, USA; The McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, USA; The Pittsburgh Institute for Neurodegenerative Diseases, University of Pittsburgh, Pittsburgh, PA, USA; The Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA. Electronic address: ctc4@pitt.edu.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Biochimica et biophysica acta</title><idno type="ISSN">0006-3002</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>Calcium (metabolism)</term><term>Cells, Cultured</term><term>Dendrites (drug effects)</term><term>Dendrites (physiology)</term><term>Dopamine Agents (pharmacology)</term><term>Electrophysiology</term><term>Female</term><term>Glutamates (metabolism)</term><term>Immunoenzyme Techniques</term><term>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</term><term>Memantine (pharmacology)</term><term>Mutation (genetics)</term><term>Neurons (drug effects)</term><term>Neurons (physiology)</term><term>Protein-Serine-Threonine Kinases (genetics)</term><term>Protein-Serine-Threonine Kinases (metabolism)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Signal Transduction (drug effects)</term><term>Synapses (drug effects)</term><term>Synapses (physiology)</term><term>Synaptosomes (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Protein-Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Calcium</term><term>Glutamates</term><term>Protein-Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Dendrites</term><term>Neurons</term><term>Signal Transduction</term><term>Synapses</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Dopamine Agents</term><term>Memantine</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Dendrites</term><term>Neurons</term><term>Synapses</term><term>Synaptosomes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Electrophysiology</term><term>Female</term><term>Immunoenzyme Techniques</term><term>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mutations in leucine-rich repeat kinase 2 (LRRK2), which are associated with autosomal dominant Parkinson's disease, elicit progressive dendrite degeneration in neurons. We hypothesized that synaptic dysregulation contributes to mutant LRRK2-induced dendritic injury. We performed in vitro whole-cell voltage clamp studies of glutamatergic receptor agonist responses and glutamatergic synaptic activity in cultured rat cortical neurons expressing full-length wild-type and mutant forms of LRRK2. Expression of the pathogenic G2019S or R1441C LRRK2 mutants resulted in larger whole-cell current responses to direct application of AMPA and NMDA receptor agonists. In addition, mutant LRRK2-expressing neurons exhibited an increased frequency of spontaneous miniature excitatory postsynaptic currents (mEPSCs) in conjunction with increased excitatory synapse density as assessed by immunofluorescence for PSD95 and VGLUT1. Mutant LRRK2-expressing neurons showed enhanced vulnerability to acute synaptic glutamate stress. Furthermore, treatment with the NMDA receptor antagonist memantine significantly protected against subsequent losses in dendrite length and branching complexity. These data demonstrate an early association between mutant LRRK2 and increased excitatory synapse activity, implicating an excitotoxic contribution to mutant LRRK2 induced dendrite degeneration.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24874075</PMID><DateCreated><Year>2014</Year><Month>08</Month><Day>05</Day></DateCreated><DateCompleted><Year>2014</Year><Month>09</Month><Day>25</Day></DateCompleted><DateRevised><Year>2017</Year><Month>05</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0006-3002</ISSN><JournalIssue CitedMedium="Print"><Volume>1842</Volume><Issue>9</Issue><PubDate><Year>2014</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Biochimica et biophysica acta</Title><ISOAbbreviation>Biochim. Biophys. Acta</ISOAbbreviation></Journal><ArticleTitle>Mutant LRRK2 enhances glutamatergic synapse activity and evokes excitotoxic dendrite degeneration.</ArticleTitle><Pagination><MedlinePgn>1596-603</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbadis.2014.05.016</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0925-4439(14)00144-6</ELocationID><Abstract><AbstractText>Mutations in leucine-rich repeat kinase 2 (LRRK2), which are associated with autosomal dominant Parkinson's disease, elicit progressive dendrite degeneration in neurons. We hypothesized that synaptic dysregulation contributes to mutant LRRK2-induced dendritic injury. We performed in vitro whole-cell voltage clamp studies of glutamatergic receptor agonist responses and glutamatergic synaptic activity in cultured rat cortical neurons expressing full-length wild-type and mutant forms of LRRK2. Expression of the pathogenic G2019S or R1441C LRRK2 mutants resulted in larger whole-cell current responses to direct application of AMPA and NMDA receptor agonists. In addition, mutant LRRK2-expressing neurons exhibited an increased frequency of spontaneous miniature excitatory postsynaptic currents (mEPSCs) in conjunction with increased excitatory synapse density as assessed by immunofluorescence for PSD95 and VGLUT1. Mutant LRRK2-expressing neurons showed enhanced vulnerability to acute synaptic glutamate stress. Furthermore, treatment with the NMDA receptor antagonist memantine significantly protected against subsequent losses in dendrite length and branching complexity. These data demonstrate an early association between mutant LRRK2 and increased excitatory synapse activity, implicating an excitotoxic contribution to mutant LRRK2 induced dendrite degeneration.</AbstractText><CopyrightInformation>Copyright © 2014 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Plowey</LastName><ForeName>Edward D</ForeName><Initials>ED</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Pathology, Stanford University, Stanford, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Johnson</LastName><ForeName>Jon W</ForeName><Initials>JW</Initials><AffiliationInfo><Affiliation>Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA; Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA; The Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Steer</LastName><ForeName>Erin</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Wan</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Pathology, Stanford University, Stanford, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eisenberg</LastName><ForeName>David A</ForeName><Initials>DA</Initials><AffiliationInfo><Affiliation>Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Valentino</LastName><ForeName>Natalie M</ForeName><Initials>NM</Initials><AffiliationInfo><Affiliation>Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Yong-Jian</ForeName><Initials>YJ</Initials><AffiliationInfo><Affiliation>Department of Physiology, Nanjing Medical University, Nanjing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chu</LastName><ForeName>Charleen T</ForeName><Initials>CT</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Ophthalmology, University of Pittsburgh, Pittsburgh, PA, USA; The McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, USA; The Pittsburgh Institute for Neurodegenerative Diseases, University of Pittsburgh, Pittsburgh, PA, USA; The Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA. Electronic address: ctc4@pitt.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>T32 NS007391</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01AG026389</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS065789</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH045817</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01MH045817</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32NS07391</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01NS065789</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K08 NS085324</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 NS074056</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AG026389</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21NS074056</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>05</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Biochim Biophys Acta</MedlineTA><NlmUniqueID>0217513</NlmUniqueID><ISSNLinking>0006-3002</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015259">Dopamine Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005971">Glutamates</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="C547428">LRRK2 protein, rat</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D000071158">Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D017346">Protein-Serine-Threonine 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