Activation of bitter taste receptors in pulmonary nociceptors sensitizes TRPV1 channels through the PLC and PKC signaling pathway.
Identifieur interne : 000D29 ( Main/Exploration ); précédent : 000D28; suivant : 000D30Activation of bitter taste receptors in pulmonary nociceptors sensitizes TRPV1 channels through the PLC and PKC signaling pathway.
Auteurs : Qihai David Gu [États-Unis] ; Deanna S. Joe [Géorgie (pays)] ; Carolyn A. Gilbert [Géorgie (pays)]Source :
- American journal of physiology. Lung cellular and molecular physiology [ 1522-1504 ] ; 2017.
Descripteurs français
- KwdFr :
- Anesthésie, Animaux, Benzophénanthridines (pharmacologie), Canaux cationiques TRPV (métabolisme), Capsaïcine (pharmacologie), Cellules réceptrices sensorielles (), Cellules réceptrices sensorielles (métabolisme), Chloroquine (administration et posologie), Chloroquine (pharmacologie), Goût (), Nocicepteurs (métabolisme), Oestrènes (pharmacologie), Perfusions veineuses, Poumon (métabolisme), Protéine kinase C (métabolisme), Pyrrolidones (pharmacologie), Rat Sprague-Dawley, Respiration (), Récepteurs couplés aux protéines G (métabolisme), Réflexe (), Transduction du signal (), Type C Phospholipases (antagonistes et inhibiteurs), Type C Phospholipases (métabolisme).
- MESH :
- administration et posologie : Chloroquine.
- antagonistes et inhibiteurs : Type C Phospholipases.
- métabolisme : Canaux cationiques TRPV, Cellules réceptrices sensorielles, Nocicepteurs, Poumon, Protéine kinase C, Récepteurs couplés aux protéines G, Type C Phospholipases.
- pharmacologie : Benzophénanthridines, Capsaïcine, Chloroquine, Oestrènes, Pyrrolidones.
- Anesthésie, Animaux, Cellules réceptrices sensorielles, Goût, Perfusions veineuses, Rat Sprague-Dawley, Respiration, Réflexe, Transduction du signal.
English descriptors
- KwdEn :
- Anesthesia, Animals, Benzophenanthridines (pharmacology), Capsaicin (pharmacology), Chloroquine (administration & dosage), Chloroquine (pharmacology), Estrenes (pharmacology), Infusions, Intravenous, Lung (metabolism), Nociceptors (metabolism), Protein Kinase C (metabolism), Pyrrolidinones (pharmacology), Rats, Sprague-Dawley, Receptors, G-Protein-Coupled (metabolism), Reflex (drug effects), Respiration (drug effects), Sensory Receptor Cells (drug effects), Sensory Receptor Cells (metabolism), Signal Transduction (drug effects), TRPV Cation Channels (metabolism), Taste (drug effects), Type C Phospholipases (antagonists & inhibitors), Type C Phospholipases (metabolism).
- MESH :
- chemical , administration & dosage : Chloroquine.
- chemical , antagonists & inhibitors : Type C Phospholipases.
- chemical , metabolism : Protein Kinase C, Receptors, G-Protein-Coupled, TRPV Cation Channels, Type C Phospholipases.
- chemical , pharmacology : Benzophenanthridines, Capsaicin, Chloroquine, Estrenes, Pyrrolidinones.
- drug effects : Reflex, Respiration, Sensory Receptor Cells, Signal Transduction, Taste.
- metabolism : Lung, Nociceptors, Sensory Receptor Cells.
- Anesthesia, Animals, Infusions, Intravenous, Rats, Sprague-Dawley.
Abstract
Bitter taste receptors (T2Rs), a G protein-coupled receptor family capable of detecting numerous bitter-tasting compounds, have recently been shown to be expressed and play diverse roles in many extraoral tissues. Here we report the functional expression of T2Rs in rat pulmonary sensory neurons. In anesthetized spontaneously breathing rats, intratracheal instillation of T2R agonist chloroquine (10 mM, 0.1 ml) significantly augmented chemoreflexes evoked by right-atrial injection of capsaicin, a specific activator for transient receptor potential vanilloid receptor 1 (TRPV1), whereas intravenous infusion of chloroquine failed to significantly affect capsaicin-evoked reflexes. In patch-clamp recordings with isolated rat vagal pulmonary sensory neurons, pretreatment with chloroquine (1-1,000 µM, 90 s) concentration dependently potentiated capsaicin-induced TRPV1-mediated inward currents. Preincubating with diphenitol and denatonium (1 mM, 90 s), two other T2R activators, also enhanced capsaicin currents in these neurons but to a lesser extent. The sensitizing effect of chloroquine was effectively prevented by the phospholipase C inhibitor U73122 (1 µM) or by the protein kinase C inhibitor chelerythrine (10 µM). In summary, our study showed that activation of T2Rs augments capsaicin-evoked TRPV1 responses in rat pulmonary nociceptors through the phospholipase C and protein kinase C signaling pathway.
DOI: 10.1152/ajplung.00468.2016
PubMed: 28062485
Affiliations:
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Le document en format XML
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Joe</name><affiliation wicri:level="1"><nlm:affiliation>Division of Basic Medical Sciences, Mercer University School of Medicine, Macon, Georgia.</nlm:affiliation><country xml:lang="fr">Géorgie (pays)</country><wicri:regionArea>Division of Basic Medical Sciences, Mercer University School of Medicine, Macon</wicri:regionArea><wicri:noRegion>Macon</wicri:noRegion></affiliation></author><author><name sortKey="Gilbert, Carolyn A" sort="Gilbert, Carolyn A" uniqKey="Gilbert C" first="Carolyn A" last="Gilbert">Carolyn A. Gilbert</name><affiliation wicri:level="1"><nlm:affiliation>Division of Basic Medical Sciences, Mercer University School of Medicine, Macon, Georgia.</nlm:affiliation><country xml:lang="fr">Géorgie (pays)</country><wicri:regionArea>Division of Basic Medical Sciences, Mercer University School of Medicine, Macon</wicri:regionArea><wicri:noRegion>Macon</wicri:noRegion></affiliation></author></analytic><series><title level="j">American journal of physiology. Lung cellular and molecular physiology</title><idno type="eISSN">1522-1504</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Anesthesia</term><term>Animals</term><term>Benzophenanthridines (pharmacology)</term><term>Capsaicin (pharmacology)</term><term>Chloroquine (administration & dosage)</term><term>Chloroquine (pharmacology)</term><term>Estrenes (pharmacology)</term><term>Infusions, Intravenous</term><term>Lung (metabolism)</term><term>Nociceptors (metabolism)</term><term>Protein Kinase C (metabolism)</term><term>Pyrrolidinones (pharmacology)</term><term>Rats, Sprague-Dawley</term><term>Receptors, G-Protein-Coupled (metabolism)</term><term>Reflex (drug effects)</term><term>Respiration (drug effects)</term><term>Sensory Receptor Cells (drug effects)</term><term>Sensory Receptor Cells (metabolism)</term><term>Signal Transduction (drug effects)</term><term>TRPV Cation Channels (metabolism)</term><term>Taste (drug effects)</term><term>Type C Phospholipases (antagonists & inhibitors)</term><term>Type C Phospholipases (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Anesthésie</term><term>Animaux</term><term>Benzophénanthridines (pharmacologie)</term><term>Canaux cationiques TRPV (métabolisme)</term><term>Capsaïcine (pharmacologie)</term><term>Cellules réceptrices sensorielles ()</term><term>Cellules réceptrices sensorielles (métabolisme)</term><term>Chloroquine (administration et posologie)</term><term>Chloroquine (pharmacologie)</term><term>Goût ()</term><term>Nocicepteurs (métabolisme)</term><term>Oestrènes (pharmacologie)</term><term>Perfusions veineuses</term><term>Poumon (métabolisme)</term><term>Protéine kinase C (métabolisme)</term><term>Pyrrolidones (pharmacologie)</term><term>Rat Sprague-Dawley</term><term>Respiration ()</term><term>Récepteurs couplés aux protéines G (métabolisme)</term><term>Réflexe ()</term><term>Transduction du signal ()</term><term>Type C Phospholipases (antagonistes et inhibiteurs)</term><term>Type C Phospholipases (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Chloroquine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Type C Phospholipases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Protein Kinase C</term><term>Receptors, G-Protein-Coupled</term><term>TRPV Cation Channels</term><term>Type C Phospholipases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Benzophenanthridines</term><term>Capsaicin</term><term>Chloroquine</term><term>Estrenes</term><term>Pyrrolidinones</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Type C Phospholipases</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Reflex</term><term>Respiration</term><term>Sensory Receptor Cells</term><term>Signal Transduction</term><term>Taste</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung</term><term>Nociceptors</term><term>Sensory Receptor Cells</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Canaux cationiques TRPV</term><term>Cellules réceptrices sensorielles</term><term>Nocicepteurs</term><term>Poumon</term><term>Protéine kinase C</term><term>Récepteurs couplés aux protéines G</term><term>Type C Phospholipases</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Benzophénanthridines</term><term>Capsaïcine</term><term>Chloroquine</term><term>Oestrènes</term><term>Pyrrolidones</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Anesthesia</term><term>Animals</term><term>Infusions, Intravenous</term><term>Rats, Sprague-Dawley</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Anesthésie</term><term>Animaux</term><term>Cellules réceptrices sensorielles</term><term>Goût</term><term>Perfusions veineuses</term><term>Rat Sprague-Dawley</term><term>Respiration</term><term>Réflexe</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Bitter taste receptors (T2Rs), a G protein-coupled receptor family capable of detecting numerous bitter-tasting compounds, have recently been shown to be expressed and play diverse roles in many extraoral tissues. Here we report the functional expression of T2Rs in rat pulmonary sensory neurons. In anesthetized spontaneously breathing rats, intratracheal instillation of T2R agonist chloroquine (10 mM, 0.1 ml) significantly augmented chemoreflexes evoked by right-atrial injection of capsaicin, a specific activator for transient receptor potential vanilloid receptor 1 (TRPV1), whereas intravenous infusion of chloroquine failed to significantly affect capsaicin-evoked reflexes. In patch-clamp recordings with isolated rat vagal pulmonary sensory neurons, pretreatment with chloroquine (1-1,000 µM, 90 s) concentration dependently potentiated capsaicin-induced TRPV1-mediated inward currents. Preincubating with diphenitol and denatonium (1 mM, 90 s), two other T2R activators, also enhanced capsaicin currents in these neurons but to a lesser extent. The sensitizing effect of chloroquine was effectively prevented by the phospholipase C inhibitor U73122 (1 µM) or by the protein kinase C inhibitor chelerythrine (10 µM). In summary, our study showed that activation of T2Rs augments capsaicin-evoked TRPV1 responses in rat pulmonary nociceptors through the phospholipase C and protein kinase C signaling pathway.</div></front></TEI><affiliations><list><country><li>Géorgie (pays)</li><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Gu, Qihai David" sort="Gu, Qihai David" uniqKey="Gu Q" first="Qihai David" last="Gu">Qihai David Gu</name></noRegion></country><country name="Géorgie (pays)"><noRegion><name sortKey="Joe, Deanna S" sort="Joe, Deanna S" uniqKey="Joe D" first="Deanna S" last="Joe">Deanna S. Joe</name></noRegion><name sortKey="Gilbert, Carolyn A" sort="Gilbert, Carolyn A" uniqKey="Gilbert C" first="Carolyn A" last="Gilbert">Carolyn A. 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