Activity-dependent hyperpolarization of EGABA is absent in cutaneous DRG neurons from inflamed rats.
Identifieur interne : 004091 ( Main/Exploration ); précédent : 004090; suivant : 004092Activity-dependent hyperpolarization of EGABA is absent in cutaneous DRG neurons from inflamed rats.
Auteurs : Y. Zhu [États-Unis] ; X-L Zhang [États-Unis] ; M S Gold [États-Unis]Source :
- Neuroscience [ 1873-7544 ] ; 2014.
Descripteurs français
- KwdFr :
- Acide 4,4'-diisothiocyano-stilbène-2,2'-disulfonique (pharmacologie), Acide gamma-amino-butyrique (pharmacologie), Acides aminés, Acides phosphiniques (pharmacologie), Adjuvant Freund, Agents GABA (pharmacologie), Animaux, Bumétanide (pharmacologie), Ganglions sensitifs des nerfs spinaux (anatomopathologie), Ganglions sensitifs des nerfs spinaux (cytologie), Inflammation (), Inflammation (anatomopathologie), Inhibiteurs du symport chlorure potassium sodium (pharmacologie), Modèles animaux de maladie humaine, Mâle, Neurones (), Neurones (physiologie), Peau (anatomopathologie), Potentiels d'action (), Potentiels d'action (physiologie), Propanolamines (pharmacologie), Rat Sprague-Dawley, Rats, Récepteurs GABA-A (génétique), Récepteurs GABA-A (métabolisme), Stimulation électrique.
- MESH :
- anatomopathologie : Ganglions sensitifs des nerfs spinaux, Inflammation, Peau.
- cytologie : Ganglions sensitifs des nerfs spinaux.
- génétique : Récepteurs GABA-A.
- métabolisme : Récepteurs GABA-A.
- pharmacologie : Acide 4,4'-diisothiocyano-stilbène-2,2'-disulfonique, Acide gamma-amino-butyrique, Acides phosphiniques, Agents GABA, Bumétanide, Inhibiteurs du symport chlorure potassium sodium, Propanolamines.
- physiologie : Neurones, Potentiels d'action.
- Acides aminés, Adjuvant Freund, Animaux, Inflammation, Modèles animaux de maladie humaine, Mâle, Neurones, Potentiels d'action, Rat Sprague-Dawley, Rats, Stimulation électrique.
English descriptors
- KwdEn :
- 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid (pharmacology), Action Potentials (drug effects), Action Potentials (physiology), Amino Acids, Animals, Bumetanide (pharmacology), Disease Models, Animal, Electric Stimulation, Freund's Adjuvant, GABA Agents (pharmacology), Ganglia, Spinal (cytology), Ganglia, Spinal (pathology), Inflammation (chemically induced), Inflammation (pathology), Male, Neurons (drug effects), Neurons (physiology), Phosphinic Acids (pharmacology), Propanolamines (pharmacology), Rats, Rats, Sprague-Dawley, Receptors, GABA-A (genetics), Receptors, GABA-A (metabolism), Skin (pathology), Sodium Potassium Chloride Symporter Inhibitors (pharmacology), gamma-Aminobutyric Acid (pharmacology).
- MESH :
- chemical , genetics : Receptors, GABA-A.
- chemical , metabolism : Receptors, GABA-A.
- chemical , pharmacology : 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid, Bumetanide, GABA Agents, Phosphinic Acids, Propanolamines, Sodium Potassium Chloride Symporter Inhibitors, gamma-Aminobutyric Acid.
- chemically induced : Inflammation.
- cytology : Ganglia, Spinal.
- drug effects : Action Potentials, Neurons.
- pathology : Ganglia, Spinal, Inflammation, Skin.
- physiology : Action Potentials, Neurons.
- chemical : Amino Acids, Animals, Disease Models, Animal, Electric Stimulation, Freund's Adjuvant, Male, Rats, Rats, Sprague-Dawley.
Abstract
A shift in GABA(A) signaling from inhibition to excitation in primary afferent neurons appears to contribute to the inflammation-induced increase in afferent input to the CNS. An activity-dependent depolarization of the GABA(A) current equilibrium potential (E(GABA)) has been described in CNS neurons which drives a shift in GABA(A) signaling from inhibition to excitation. The purpose of the present study was to determine if such an activity-dependent depolarization of E(GABA) occurs in primary afferents and whether the depolarization is amplified with persistent inflammation. Acutely dissociated retrogradely labeled cutaneous dorsal root ganglion (DRG) neurons from naïve and inflamed rats were studied with gramicidin perforated patch recording. Rather than a depolarization, 200 action potentials delivered at 2 Hz resulted in a ∼10 mV hyperpolarization of E(GABA) in cutaneous neurons from naïve rats. No such hyperpolarization was observed in neurons from inflamed rats. The shift in E(GABA) was not blocked by 10 μM bumetanide. Furthermore, because activity-dependent hyperpolarization of E(GABA) was fully manifest in the absence of HCO₃⁻ in the bath solution, this shift was not dependent on a change in HCO₃⁻-Cl⁻ exchanger activity, despite evidence of HCO₃⁻-Cl⁻ exchangers in DRG neurons that may contribute to the establishment of E(GABA) in the presence of HCO₃⁻. While the mechanism underlying the activity-dependent hyperpolarization of E(GABA) has yet to be identified, because this mechanism appears to function as a form of feedback inhibition, facilitating GABA-mediated inhibition of afferent activity, it may serve as a novel target for the treatment of inflammatory pain.
DOI: 10.1016/j.neuroscience.2013.10.004
PubMed: 24135545
Affiliations:
- États-Unis
- Pennsylvanie
- College Park (Maryland), Pittsburgh
- Université de Pittsburgh, Université du Maryland
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Le document en format XML
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Zhu</name><affiliation wicri:level="4"><nlm:affiliation>Department of Neural and Pain Sciences, University of Maryland, Baltimore School of Dentistry, Baltimore, MD, USA; Department of Anesthesiology, Division of Gastroenterology Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neural and Pain Sciences, University of Maryland, Baltimore School of Dentistry, Baltimore, MD, USA; Department of Anesthesiology, Division of Gastroenterology Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA</wicri:regionArea><placeName><region type="state">Pennsylvanie</region><settlement type="city">College Park (Maryland)</settlement></placeName><orgName type="university">Université du Maryland</orgName></affiliation></author><author><name sortKey="Zhang, X L" sort="Zhang, X L" uniqKey="Zhang X" first="X-L" last="Zhang">X-L Zhang</name><affiliation wicri:level="4"><nlm:affiliation>Department of Anesthesiology, Division of Gastroenterology Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA, USA; Department of Pharmacology and Cell Biology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Anesthesiology, Division of Gastroenterology Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA, USA; Department of Pharmacology and Cell Biology, School of Medicine, University of Pittsburgh, Pittsburgh, PA</wicri:regionArea><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation></author><author><name sortKey="Gold, M S" sort="Gold, M S" uniqKey="Gold M" first="M S" last="Gold">M S Gold</name><affiliation wicri:level="4"><nlm:affiliation>Department of Anesthesiology, Division of Gastroenterology Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA, USA; Department of Neurobiology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA; Department of Medicine, Division of Gastroenterology Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA, USA; Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA; Pittsburgh Center for Pain Research, University of Pittsburgh, Pittsburgh, PA, USA. 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Zhu</name><affiliation wicri:level="4"><nlm:affiliation>Department of Neural and Pain Sciences, University of Maryland, Baltimore School of Dentistry, Baltimore, MD, USA; Department of Anesthesiology, Division of Gastroenterology Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neural and Pain Sciences, University of Maryland, Baltimore School of Dentistry, Baltimore, MD, USA; Department of Anesthesiology, Division of Gastroenterology Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA</wicri:regionArea><placeName><region type="state">Pennsylvanie</region><settlement type="city">College Park (Maryland)</settlement></placeName><orgName type="university">Université du Maryland</orgName></affiliation></author><author><name sortKey="Zhang, X L" sort="Zhang, X L" uniqKey="Zhang X" first="X-L" last="Zhang">X-L Zhang</name><affiliation wicri:level="4"><nlm:affiliation>Department of Anesthesiology, Division of Gastroenterology Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA, USA; Department of Pharmacology and Cell Biology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Anesthesiology, Division of Gastroenterology Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA, USA; Department of Pharmacology and Cell Biology, School of Medicine, University of Pittsburgh, Pittsburgh, PA</wicri:regionArea><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation></author><author><name sortKey="Gold, M S" sort="Gold, M S" uniqKey="Gold M" first="M S" last="Gold">M S Gold</name><affiliation wicri:level="4"><nlm:affiliation>Department of Anesthesiology, Division of Gastroenterology Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA, USA; Department of Neurobiology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA; Department of Medicine, Division of Gastroenterology Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA, USA; Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA; Pittsburgh Center for Pain Research, University of Pittsburgh, Pittsburgh, PA, USA. 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(metabolism)</term><term>Skin (pathology)</term><term>Sodium Potassium Chloride Symporter Inhibitors (pharmacology)</term><term>gamma-Aminobutyric Acid (pharmacology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acide 4,4'-diisothiocyano-stilbène-2,2'-disulfonique (pharmacologie)</term><term>Acide gamma-amino-butyrique (pharmacologie)</term><term>Acides aminés</term><term>Acides phosphiniques (pharmacologie)</term><term>Adjuvant Freund</term><term>Agents GABA (pharmacologie)</term><term>Animaux</term><term>Bumétanide (pharmacologie)</term><term>Ganglions sensitifs des nerfs spinaux (anatomopathologie)</term><term>Ganglions sensitifs des nerfs spinaux (cytologie)</term><term>Inflammation ()</term><term>Inflammation (anatomopathologie)</term><term>Inhibiteurs du symport chlorure potassium sodium (pharmacologie)</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Neurones ()</term><term>Neurones (physiologie)</term><term>Peau (anatomopathologie)</term><term>Potentiels d'action ()</term><term>Potentiels d'action (physiologie)</term><term>Propanolamines (pharmacologie)</term><term>Rat Sprague-Dawley</term><term>Rats</term><term>Récepteurs GABA-A (génétique)</term><term>Récepteurs GABA-A (métabolisme)</term><term>Stimulation électrique</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, GABA-A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Receptors, GABA-A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid</term><term>Bumetanide</term><term>GABA Agents</term><term>Phosphinic Acids</term><term>Propanolamines</term><term>Sodium Potassium Chloride Symporter Inhibitors</term><term>gamma-Aminobutyric Acid</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Ganglions 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4,4'-diisothiocyano-stilbène-2,2'-disulfonique</term><term>Acide gamma-amino-butyrique</term><term>Acides phosphiniques</term><term>Agents GABA</term><term>Bumétanide</term><term>Inhibiteurs du symport chlorure potassium sodium</term><term>Propanolamines</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Neurones</term><term>Potentiels d'action</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Action Potentials</term><term>Neurons</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Amino Acids</term><term>Animals</term><term>Disease Models, Animal</term><term>Electric Stimulation</term><term>Freund's Adjuvant</term><term>Male</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Acides aminés</term><term>Adjuvant Freund</term><term>Animaux</term><term>Inflammation</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Neurones</term><term>Potentiels d'action</term><term>Rat Sprague-Dawley</term><term>Rats</term><term>Stimulation électrique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A shift in GABA(A) signaling from inhibition to excitation in primary afferent neurons appears to contribute to the inflammation-induced increase in afferent input to the CNS. An activity-dependent depolarization of the GABA(A) current equilibrium potential (E(GABA)) has been described in CNS neurons which drives a shift in GABA(A) signaling from inhibition to excitation. The purpose of the present study was to determine if such an activity-dependent depolarization of E(GABA) occurs in primary afferents and whether the depolarization is amplified with persistent inflammation. Acutely dissociated retrogradely labeled cutaneous dorsal root ganglion (DRG) neurons from naïve and inflamed rats were studied with gramicidin perforated patch recording. Rather than a depolarization, 200 action potentials delivered at 2 Hz resulted in a ∼10 mV hyperpolarization of E(GABA) in cutaneous neurons from naïve rats. No such hyperpolarization was observed in neurons from inflamed rats. The shift in E(GABA) was not blocked by 10 μM bumetanide. Furthermore, because activity-dependent hyperpolarization of E(GABA) was fully manifest in the absence of HCO₃⁻ in the bath solution, this shift was not dependent on a change in HCO₃⁻-Cl⁻ exchanger activity, despite evidence of HCO₃⁻-Cl⁻ exchangers in DRG neurons that may contribute to the establishment of E(GABA) in the presence of HCO₃⁻. While the mechanism underlying the activity-dependent hyperpolarization of E(GABA) has yet to be identified, because this mechanism appears to function as a form of feedback inhibition, facilitating GABA-mediated inhibition of afferent activity, it may serve as a novel target for the treatment of inflammatory pain.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Pennsylvanie</li></region><settlement><li>College Park (Maryland)</li><li>Pittsburgh</li></settlement><orgName><li>Université de Pittsburgh</li><li>Université du Maryland</li></orgName></list><tree><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Zhu, Y" sort="Zhu, Y" uniqKey="Zhu Y" first="Y" last="Zhu">Y. Zhu</name></region><name sortKey="Gold, M S" sort="Gold, M S" uniqKey="Gold M" first="M S" last="Gold">M S Gold</name><name sortKey="Zhang, X L" sort="Zhang, X L" uniqKey="Zhang X" first="X-L" last="Zhang">X-L Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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