Transient muscarinic and glutamatergic stimulation of neural stem cells triggers acute and persistent changes in differentiation.
Identifieur interne : 001713 ( PubMed/Corpus ); précédent : 001712; suivant : 001714Transient muscarinic and glutamatergic stimulation of neural stem cells triggers acute and persistent changes in differentiation.
Auteurs : Ranmal A. Samarasinghe ; Prasad S. Kanuparthi ; J. Timothy Greenamyre ; Donald B. Defranco ; Roberto Di MaioSource :
- Neurobiology of disease [ 1095-953X ] ; 2014.
English descriptors
- KwdEn :
- Animals, Chronic Disease, Disease Models, Animal, Epilepsy (physiopathology), GABAergic Neurons (drug effects), GABAergic Neurons (physiology), Gap Junctions (drug effects), Gap Junctions (physiology), Glutamic Acid (metabolism), Hippocampus (drug effects), Hippocampus (physiopathology), Humans, Induced Pluripotent Stem Cells (drug effects), Induced Pluripotent Stem Cells (physiology), Male, Mice, Muscarinic Agonists (pharmacology), Neural Stem Cells (drug effects), Neural Stem Cells (physiology), Neurogenesis (drug effects), Neurogenesis (physiology), Pilocarpine (pharmacology), Rats, Rats, Sprague-Dawley, Receptors, Metabotropic Glutamate (metabolism), Receptors, Muscarinic (metabolism).
- MESH :
- chemical , metabolism : Glutamic Acid, Receptors, Metabotropic Glutamate, Receptors, Muscarinic.
- drug effects : GABAergic Neurons, Gap Junctions, Hippocampus, Induced Pluripotent Stem Cells, Neural Stem Cells, Neurogenesis.
- chemical , pharmacology : Muscarinic Agonists, Pilocarpine.
- physiology : GABAergic Neurons, Gap Junctions, Induced Pluripotent Stem Cells, Neural Stem Cells, Neurogenesis.
- physiopathology : Epilepsy, Hippocampus.
- Animals, Chronic Disease, Disease Models, Animal, Humans, Male, Mice, Rats, Rats, Sprague-Dawley.
Abstract
While aberrant cell proliferation and differentiation may contribute to epileptogenesis, the mechanisms linking an initial epileptic insult to subsequent changes in cell fate remain elusive. Using both mouse and human iPSC-derived neural progenitor/stem cells (NPSCs), we found that a combined transient muscarinic and mGluR1 stimulation inhibited overall neurogenesis but enhanced NPSC differentiation into immature GABAergic cells. If treated NPSCs were further passaged, they retained a nearly identical phenotype upon differentiation. A similar profusion of immature GABAergic cells was seen in rats with pilocarpine-induced chronic epilepsy. Furthermore, live cell imaging revealed abnormal de-synchrony of Ca(++) transients and altered gap junction intercellular communication following combined muscarinic/glutamatergic stimulation, which was associated with either acute site-specific dephosphorylation of connexin 43 or a long-term enhancement of its degradation. Therefore, epileptogenic stimuli can trigger acute and persistent changes in cell fate by altering distinct mechanisms that function to maintain appropriate intercellular communication between coupled NPSCs.
DOI: 10.1016/j.nbd.2014.06.020
PubMed: 25003306
Links to Exploration step
pubmed:25003306Le document en format XML
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Kanuparthi</name><affiliation><nlm:affiliation>University of Pittsburgh School of Medicine, Department of Pharmacology and Chemical Biology, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Timothy Greenamyre, J" sort="Timothy Greenamyre, J" uniqKey="Timothy Greenamyre J" first="J" last="Timothy Greenamyre">J. Timothy Greenamyre</name><affiliation><nlm:affiliation>University of Pittsburgh School of Medicine-Pittsburgh, Institute of Neurodegenerative Diseases, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Defranco, Donald B" sort="Defranco, Donald B" uniqKey="Defranco D" first="Donald B" last="Defranco">Donald B. Defranco</name><affiliation><nlm:affiliation>University of Pittsburgh School of Medicine, Department of Pharmacology and Chemical Biology, USA. Electronic address: dod1@pitt.edu.</nlm:affiliation></affiliation></author><author><name sortKey="Di Maio, Roberto" sort="Di Maio, Roberto" uniqKey="Di Maio R" first="Roberto" last="Di Maio">Roberto Di Maio</name><affiliation><nlm:affiliation>University of Pittsburgh School of Medicine-Pittsburgh, Institute of Neurodegenerative Diseases, USA.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:25003306</idno><idno type="pmid">25003306</idno><idno type="doi">10.1016/j.nbd.2014.06.020</idno><idno type="wicri:Area/PubMed/Corpus">001713</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001713</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Transient muscarinic and glutamatergic stimulation of neural stem cells triggers acute and persistent changes in differentiation.</title><author><name sortKey="Samarasinghe, Ranmal A" sort="Samarasinghe, Ranmal A" uniqKey="Samarasinghe R" first="Ranmal A" last="Samarasinghe">Ranmal A. Samarasinghe</name><affiliation><nlm:affiliation>University of Pittsburgh School of Medicine, Department of Pharmacology and Chemical Biology, USA; University of California Los Angeles, Department of Neurology, USA. Electronic address: ranmals@gmail.com.</nlm:affiliation></affiliation></author><author><name sortKey="Kanuparthi, Prasad S" sort="Kanuparthi, Prasad S" uniqKey="Kanuparthi P" first="Prasad S" last="Kanuparthi">Prasad S. Kanuparthi</name><affiliation><nlm:affiliation>University of Pittsburgh School of Medicine, Department of Pharmacology and Chemical Biology, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Timothy Greenamyre, J" sort="Timothy Greenamyre, J" uniqKey="Timothy Greenamyre J" first="J" last="Timothy Greenamyre">J. Timothy Greenamyre</name><affiliation><nlm:affiliation>University of Pittsburgh School of Medicine-Pittsburgh, Institute of Neurodegenerative Diseases, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Defranco, Donald B" sort="Defranco, Donald B" uniqKey="Defranco D" first="Donald B" last="Defranco">Donald B. Defranco</name><affiliation><nlm:affiliation>University of Pittsburgh School of Medicine, Department of Pharmacology and Chemical Biology, USA. Electronic address: dod1@pitt.edu.</nlm:affiliation></affiliation></author><author><name sortKey="Di Maio, Roberto" sort="Di Maio, Roberto" uniqKey="Di Maio R" first="Roberto" last="Di Maio">Roberto Di Maio</name><affiliation><nlm:affiliation>University of Pittsburgh School of Medicine-Pittsburgh, Institute of Neurodegenerative Diseases, USA.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Neurobiology of disease</title><idno type="eISSN">1095-953X</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>Chronic Disease</term><term>Disease Models, Animal</term><term>Epilepsy (physiopathology)</term><term>GABAergic Neurons (drug effects)</term><term>GABAergic Neurons (physiology)</term><term>Gap Junctions (drug effects)</term><term>Gap Junctions (physiology)</term><term>Glutamic Acid (metabolism)</term><term>Hippocampus (drug effects)</term><term>Hippocampus (physiopathology)</term><term>Humans</term><term>Induced Pluripotent Stem Cells (drug effects)</term><term>Induced Pluripotent Stem Cells (physiology)</term><term>Male</term><term>Mice</term><term>Muscarinic Agonists (pharmacology)</term><term>Neural Stem Cells (drug effects)</term><term>Neural Stem Cells (physiology)</term><term>Neurogenesis (drug effects)</term><term>Neurogenesis (physiology)</term><term>Pilocarpine (pharmacology)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Receptors, Metabotropic Glutamate (metabolism)</term><term>Receptors, Muscarinic (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutamic Acid</term><term>Receptors, Metabotropic Glutamate</term><term>Receptors, Muscarinic</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>GABAergic Neurons</term><term>Gap Junctions</term><term>Hippocampus</term><term>Induced Pluripotent Stem Cells</term><term>Neural Stem Cells</term><term>Neurogenesis</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Muscarinic Agonists</term><term>Pilocarpine</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>GABAergic Neurons</term><term>Gap Junctions</term><term>Induced Pluripotent Stem Cells</term><term>Neural Stem Cells</term><term>Neurogenesis</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Epilepsy</term><term>Hippocampus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Chronic Disease</term><term>Disease Models, Animal</term><term>Humans</term><term>Male</term><term>Mice</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">While aberrant cell proliferation and differentiation may contribute to epileptogenesis, the mechanisms linking an initial epileptic insult to subsequent changes in cell fate remain elusive. Using both mouse and human iPSC-derived neural progenitor/stem cells (NPSCs), we found that a combined transient muscarinic and mGluR1 stimulation inhibited overall neurogenesis but enhanced NPSC differentiation into immature GABAergic cells. If treated NPSCs were further passaged, they retained a nearly identical phenotype upon differentiation. A similar profusion of immature GABAergic cells was seen in rats with pilocarpine-induced chronic epilepsy. Furthermore, live cell imaging revealed abnormal de-synchrony of Ca(++) transients and altered gap junction intercellular communication following combined muscarinic/glutamatergic stimulation, which was associated with either acute site-specific dephosphorylation of connexin 43 or a long-term enhancement of its degradation. Therefore, epileptogenic stimuli can trigger acute and persistent changes in cell fate by altering distinct mechanisms that function to maintain appropriate intercellular communication between coupled NPSCs.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25003306</PMID><DateCreated><Year>2014</Year><Month>08</Month><Day>11</Day></DateCreated><DateCompleted><Year>2015</Year><Month>04</Month><Day>21</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-953X</ISSN><JournalIssue CitedMedium="Internet"><Volume>70</Volume><PubDate><Year>2014</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Neurobiology of disease</Title><ISOAbbreviation>Neurobiol. Dis.</ISOAbbreviation></Journal><ArticleTitle>Transient muscarinic and glutamatergic stimulation of neural stem cells triggers acute and persistent changes in differentiation.</ArticleTitle><Pagination><MedlinePgn>252-61</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.nbd.2014.06.020</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0969-9961(14)00184-3</ELocationID><Abstract><AbstractText>While aberrant cell proliferation and differentiation may contribute to epileptogenesis, the mechanisms linking an initial epileptic insult to subsequent changes in cell fate remain elusive. Using both mouse and human iPSC-derived neural progenitor/stem cells (NPSCs), we found that a combined transient muscarinic and mGluR1 stimulation inhibited overall neurogenesis but enhanced NPSC differentiation into immature GABAergic cells. If treated NPSCs were further passaged, they retained a nearly identical phenotype upon differentiation. A similar profusion of immature GABAergic cells was seen in rats with pilocarpine-induced chronic epilepsy. Furthermore, live cell imaging revealed abnormal de-synchrony of Ca(++) transients and altered gap junction intercellular communication following combined muscarinic/glutamatergic stimulation, which was associated with either acute site-specific dephosphorylation of connexin 43 or a long-term enhancement of its degradation. Therefore, epileptogenic stimuli can trigger acute and persistent changes in cell fate by altering distinct mechanisms that function to maintain appropriate intercellular communication between coupled NPSCs.</AbstractText><CopyrightInformation>Copyright © 2014 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Samarasinghe</LastName><ForeName>Ranmal A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>University of Pittsburgh School of Medicine, Department of Pharmacology and Chemical Biology, USA; University of California Los Angeles, Department of Neurology, USA. Electronic address: ranmals@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kanuparthi</LastName><ForeName>Prasad S</ForeName><Initials>PS</Initials><AffiliationInfo><Affiliation>University of Pittsburgh School of Medicine, Department of Pharmacology and Chemical Biology, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Timothy Greenamyre</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>University of Pittsburgh School of Medicine-Pittsburgh, Institute of Neurodegenerative Diseases, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>DeFranco</LastName><ForeName>Donald B</ForeName><Initials>DB</Initials><AffiliationInfo><Affiliation>University of Pittsburgh School of Medicine, Department of Pharmacology and Chemical Biology, USA. Electronic address: dod1@pitt.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Di Maio</LastName><ForeName>Roberto</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>University of Pittsburgh School of Medicine-Pittsburgh, Institute of Neurodegenerative Diseases, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>UL1 TR000005</GrantID><Acronym>TR</Acronym><Agency>NCATS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>UL1 RR024153</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>DK078394</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>1UL1 RR024153</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DK078394</GrantID><Acronym>DK</Acronym><Agency>NIDDK 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></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>07</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurobiol Dis</MedlineTA><NlmUniqueID>9500169</NlmUniqueID><ISSNLinking>0969-9961</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018721">Muscarinic Agonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018094">Receptors, Metabotropic Glutamate</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011976">Receptors, Muscarinic</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C104077">metabotropic glutamate receptor type 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>01MI4Q9DI3</RegistryNumber><NameOfSubstance UI="D010862">Pilocarpine</NameOfSubstance></Chemical><Chemical><RegistryNumber>3KX376GY7L</RegistryNumber><NameOfSubstance UI="D018698">Glutamic Acid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Trends Neurosci. 2008 May;31(5):243-50</RefSource><PMID Version="1">18403031</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Stem Cells. 2008 Apr;26(4):988-96</RefSource><PMID Version="1">18218818</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroscientist. 2008 Oct;14(5):446-58</RefSource><PMID Version="1">18997123</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Rev Neurol. 2009 Jul;5(7):380-91</RefSource><PMID 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MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010862" MajorTopicYN="N">Pilocarpine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018094" MajorTopicYN="N">Receptors, Metabotropic Glutamate</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011976" MajorTopicYN="N">Receptors, Muscarinic</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">NIHMS612531</OtherID><OtherID Source="NLM">PMC4152385</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Connexin</Keyword><Keyword 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|étape= Corpus
|type= RBID
|clé= pubmed:25003306
|texte= Transient muscarinic and glutamatergic stimulation of neural stem cells triggers acute and persistent changes in differentiation.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:25003306" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a PittsburghV1
| This area was generated with Dilib version V0.6.38. |  |