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Newborn Analgesia Mediated by Oxytocin during Delivery

The mechanisms controlling pain in newborns during delivery are poorly understood. We explored the hypothesis that oxytocin, an essential hormone for labor and a powerful neuromodulator, exerts analgesic actions on newborns during delivery. Using a thermal tail-flick assay, we report that pain sensi...

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Autores principales: Mazzuca, Michel, Minlebaev, Marat, Shakirzyanova, Anastasia, Tyzio, Roman, Taccola, Giuliano, Janackova, Sona, Gataullina, Svetlana, Ben-Ari, Yehezkel, Giniatullin, Rashid, Khazipov, Rustem
Formato: Texto
Lenguaje:English
Publicado: Frontiers Research Foundation 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3080614/
https://www.ncbi.nlm.nih.gov/pubmed/21519396
http://dx.doi.org/10.3389/fncel.2011.00003
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author Mazzuca, Michel
Minlebaev, Marat
Shakirzyanova, Anastasia
Tyzio, Roman
Taccola, Giuliano
Janackova, Sona
Gataullina, Svetlana
Ben-Ari, Yehezkel
Giniatullin, Rashid
Khazipov, Rustem
author_facet Mazzuca, Michel
Minlebaev, Marat
Shakirzyanova, Anastasia
Tyzio, Roman
Taccola, Giuliano
Janackova, Sona
Gataullina, Svetlana
Ben-Ari, Yehezkel
Giniatullin, Rashid
Khazipov, Rustem
author_sort Mazzuca, Michel
collection PubMed
description The mechanisms controlling pain in newborns during delivery are poorly understood. We explored the hypothesis that oxytocin, an essential hormone for labor and a powerful neuromodulator, exerts analgesic actions on newborns during delivery. Using a thermal tail-flick assay, we report that pain sensitivity is two-fold lower in rat pups immediately after birth than 2 days later. Oxytocin receptor antagonists strongly enhanced pain sensitivity in newborn, but not in 2-day-old rats, whereas oxytocin reduced pain at both ages suggesting an endogenous analgesia by oxytocin during delivery. Similar analgesic effects of oxytocin, measured as attenuation of pain-vocalization induced by electrical whisker pad stimulation, were also observed in decerebrated newborns. Oxytocin reduced GABA-evoked calcium responses and depolarizing GABA driving force in isolated neonatal trigeminal neurons suggesting that oxytocin effects are mediated by alterations of intracellular chloride. Unlike GABA signaling, oxytocin did not affect responses mediated by P2X3 and TRPV1 receptors. In keeping with a GABAergic mechanism, reduction of intracellular chloride by the diuretic NKCC1 chloride co-transporter antagonist bumetanide mimicked the analgesic actions of oxytocin and its effects on GABA responses in nociceptive neurons. Therefore, endogenous oxytocin exerts an analgesic action in newborn pups that involves a reduction of the depolarizing action of GABA on nociceptive neurons. Therefore, the same hormone that triggers delivery also acts as a natural pain killer revealing a novel facet of the protective actions of oxytocin in the fetus at birth.
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spelling pubmed-30806142011-04-25 Newborn Analgesia Mediated by Oxytocin during Delivery Mazzuca, Michel Minlebaev, Marat Shakirzyanova, Anastasia Tyzio, Roman Taccola, Giuliano Janackova, Sona Gataullina, Svetlana Ben-Ari, Yehezkel Giniatullin, Rashid Khazipov, Rustem Front Cell Neurosci Neuroscience The mechanisms controlling pain in newborns during delivery are poorly understood. We explored the hypothesis that oxytocin, an essential hormone for labor and a powerful neuromodulator, exerts analgesic actions on newborns during delivery. Using a thermal tail-flick assay, we report that pain sensitivity is two-fold lower in rat pups immediately after birth than 2 days later. Oxytocin receptor antagonists strongly enhanced pain sensitivity in newborn, but not in 2-day-old rats, whereas oxytocin reduced pain at both ages suggesting an endogenous analgesia by oxytocin during delivery. Similar analgesic effects of oxytocin, measured as attenuation of pain-vocalization induced by electrical whisker pad stimulation, were also observed in decerebrated newborns. Oxytocin reduced GABA-evoked calcium responses and depolarizing GABA driving force in isolated neonatal trigeminal neurons suggesting that oxytocin effects are mediated by alterations of intracellular chloride. Unlike GABA signaling, oxytocin did not affect responses mediated by P2X3 and TRPV1 receptors. In keeping with a GABAergic mechanism, reduction of intracellular chloride by the diuretic NKCC1 chloride co-transporter antagonist bumetanide mimicked the analgesic actions of oxytocin and its effects on GABA responses in nociceptive neurons. Therefore, endogenous oxytocin exerts an analgesic action in newborn pups that involves a reduction of the depolarizing action of GABA on nociceptive neurons. Therefore, the same hormone that triggers delivery also acts as a natural pain killer revealing a novel facet of the protective actions of oxytocin in the fetus at birth. Frontiers Research Foundation 2011-04-12 /pmc/articles/PMC3080614/ /pubmed/21519396 http://dx.doi.org/10.3389/fncel.2011.00003 Text en Copyright © 2011 Mazzuca, Minlebaev, Shakirzyanova, Tyzio, Taccola, Janackova, Gataullina, Ben-Ari, Giniatullin and Khazipov. http://www.frontiersin.org/licenseagreement This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with.
spellingShingle Neuroscience
Mazzuca, Michel
Minlebaev, Marat
Shakirzyanova, Anastasia
Tyzio, Roman
Taccola, Giuliano
Janackova, Sona
Gataullina, Svetlana
Ben-Ari, Yehezkel
Giniatullin, Rashid
Khazipov, Rustem
Newborn Analgesia Mediated by Oxytocin during Delivery
title Newborn Analgesia Mediated by Oxytocin during Delivery
title_full Newborn Analgesia Mediated by Oxytocin during Delivery
title_fullStr Newborn Analgesia Mediated by Oxytocin during Delivery
title_full_unstemmed Newborn Analgesia Mediated by Oxytocin during Delivery
title_short Newborn Analgesia Mediated by Oxytocin during Delivery
title_sort newborn analgesia mediated by oxytocin during delivery
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3080614/
https://www.ncbi.nlm.nih.gov/pubmed/21519396
http://dx.doi.org/10.3389/fncel.2011.00003
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