Transient Muscarinic and Glutamatergic Stimulation of Neural Stem Cells Trigger Acute and Persistent Changes in Differentiation
Identifieur interne : 000B07 ( Main/Exploration ); précédent : 000B06; suivant : 000B08Transient Muscarinic and Glutamatergic Stimulation of Neural Stem Cells Trigger 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 [ 0969-9961 ] ; 2014.
Descripteurs français
- KwdFr :
- Acide glutamique (métabolisme), Agonistes muscariniques (pharmacologie), Animaux, Cellules souches neurales (), Cellules souches neurales (physiologie), Cellules souches pluripotentes induites (), Cellules souches pluripotentes induites (physiologie), Hippocampe (), Hippocampe (physiopathologie), Humains, Jonctions communicantes (), Jonctions communicantes (physiologie), Maladie chronique, Modèles animaux de maladie humaine, Mâle, Neurogenèse (), Neurogenèse (physiologie), Neurones GABAergiques (), Neurones GABAergiques (physiologie), Pilocarpine (pharmacologie), Rat Sprague-Dawley, Rats, Récepteur muscarinique (métabolisme), Récepteurs métabotropes au glutamate (métabolisme), Souris, Épilepsie (physiopathologie).
- MESH :
- métabolisme : Acide glutamique, Récepteur muscarinique, Récepteurs métabotropes au glutamate.
- pharmacologie : Agonistes muscariniques, Pilocarpine.
- physiologie : Cellules souches neurales, Cellules souches pluripotentes induites, Jonctions communicantes, Neurogenèse, Neurones GABAergiques.
- physiopathologie : Hippocampe, Épilepsie.
- Animaux, Cellules souches neurales, Cellules souches pluripotentes induites, Hippocampe, Humains, Jonctions communicantes, Maladie chronique, Modèles animaux de maladie humaine, Mâle, Neurogenèse, Neurones GABAergiques, Rat Sprague-Dawley, Rats, Souris.
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.
Url:
DOI: 10.1016/j.nbd.2014.06.020
PubMed: 25003306
PubMed Central: 4152385
Affiliations:
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Samarasinghe</name><affiliation><nlm:aff id="A1">University of Pittsburgh School of Medicine Department of Pharmacology and Chemical Biology</nlm:aff></affiliation><affiliation><nlm:aff id="A2">University of California Los Angeles, Department of Neurology</nlm:aff><wicri:noCountry code="subfield">Department of Neurology</wicri:noCountry></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:aff id="A1">University of Pittsburgh School of Medicine Department of Pharmacology and Chemical Biology</nlm:aff></affiliation></author><author><name sortKey="Greenamyre, J Timothy" sort="Greenamyre, J Timothy" uniqKey="Greenamyre J" first="J. Timothy" last="Greenamyre">J. 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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="KwdFr" xml:lang="fr"><term>Acide glutamique (métabolisme)</term><term>Agonistes muscariniques (pharmacologie)</term><term>Animaux</term><term>Cellules souches neurales ()</term><term>Cellules souches neurales (physiologie)</term><term>Cellules souches pluripotentes induites ()</term><term>Cellules souches pluripotentes induites (physiologie)</term><term>Hippocampe ()</term><term>Hippocampe (physiopathologie)</term><term>Humains</term><term>Jonctions communicantes ()</term><term>Jonctions communicantes (physiologie)</term><term>Maladie chronique</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Neurogenèse ()</term><term>Neurogenèse (physiologie)</term><term>Neurones GABAergiques ()</term><term>Neurones GABAergiques (physiologie)</term><term>Pilocarpine (pharmacologie)</term><term>Rat Sprague-Dawley</term><term>Rats</term><term>Récepteur muscarinique (métabolisme)</term><term>Récepteurs métabotropes au glutamate (métabolisme)</term><term>Souris</term><term>Épilepsie (physiopathologie)</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" qualifier="métabolisme" xml:lang="fr"><term>Acide glutamique</term><term>Récepteur muscarinique</term><term>Récepteurs métabotropes au glutamate</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Agonistes muscariniques</term><term>Pilocarpine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Muscarinic Agonists</term><term>Pilocarpine</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Cellules souches neurales</term><term>Cellules souches pluripotentes induites</term><term>Jonctions communicantes</term><term>Neurogenèse</term><term>Neurones GABAergiques</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="physiopathologie" xml:lang="fr"><term>Hippocampe</term><term>Épilepsie</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><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules souches neurales</term><term>Cellules souches pluripotentes induites</term><term>Hippocampe</term><term>Humains</term><term>Jonctions communicantes</term><term>Maladie chronique</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Neurogenèse</term><term>Neurones GABAergiques</term><term>Rat Sprague-Dawley</term><term>Rats</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">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<sup>++</sup> 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.</p></div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Defranco, Donald B" sort="Defranco, Donald B" uniqKey="Defranco D" first="Donald B." last="Defranco">Donald B. Defranco</name><name sortKey="Di Maio, Roberto" sort="Di Maio, Roberto" uniqKey="Di Maio R" first="Roberto" last="Di Maio">Roberto Di Maio</name><name sortKey="Greenamyre, J Timothy" sort="Greenamyre, J Timothy" uniqKey="Greenamyre J" first="J. Timothy" last="Greenamyre">J. Timothy Greenamyre</name><name sortKey="Kanuparthi, Prasad S" sort="Kanuparthi, Prasad S" uniqKey="Kanuparthi P" first="Prasad S." last="Kanuparthi">Prasad S. Kanuparthi</name><name sortKey="Samarasinghe, Ranmal A" sort="Samarasinghe, Ranmal A" uniqKey="Samarasinghe R" first="Ranmal A." last="Samarasinghe">Ranmal A. 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