Sensitization of neonatal rat lumbar motoneuron by the inflammatory pain mediator bradykinin
Bradykinin (Bk) is a potent inflammatory mediator that causes hyperalgesia. The action of Bk on the sensory system is well documented but its effects on motoneurons, the final pathway of the motor system, are unknown. By a combination of patch-clamp recordings and two-photon calcium imaging, we foun...
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doaj-e853f6392de545cebd6a56699cfd96e92021-05-04T23:42:08ZengeLife Sciences Publications LtdeLife2050-084X2015-03-01410.7554/eLife.06195Sensitization of neonatal rat lumbar motoneuron by the inflammatory pain mediator bradykininMouloud Bouhadfane0Attila Kaszás1Balázs Rózsa2Ronald M Harris-Warrick3Laurent Vinay4Frédéric Brocard5Institut de Neurosciences de la Timone (UMR7289), Aix-Marseille Université and CNRS, Marseille, FranceInstitut de Neuroscience des Systèmes (UMR1106), Aix Marseille Université and INSERM, Marseille, FranceTwo-Photon Imaging Center, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary; Faculty of Information Technology and Bionics, Pázmány Péter Catholic University, Budapest, HungaryDepartment of Neurobiology and Behavior, Cornell University, Ithaca, United StatesInstitut de Neurosciences de la Timone (UMR7289), Aix-Marseille Université and CNRS, Marseille, FranceInstitut de Neurosciences de la Timone (UMR7289), Aix-Marseille Université and CNRS, Marseille, FranceBradykinin (Bk) is a potent inflammatory mediator that causes hyperalgesia. The action of Bk on the sensory system is well documented but its effects on motoneurons, the final pathway of the motor system, are unknown. By a combination of patch-clamp recordings and two-photon calcium imaging, we found that Bk strongly sensitizes spinal motoneurons. Sensitization was characterized by an increased ability to generate self-sustained spiking in response to excitatory inputs. Our pharmacological study described a dual ionic mechanism to sensitize motoneurons, including inhibition of a barium-sensitive resting K+ conductance and activation of a nonselective cationic conductance primarily mediated by Na+. Examination of the upstream signaling pathways provided evidence for postsynaptic activation of B2 receptors, G protein activation of phospholipase C, InsP3 synthesis, and calmodulin activation. This study questions the influence of motoneurons in the assessment of hyperalgesia since the withdrawal motor reflex is commonly used as a surrogate pain model.https://elifesciences.org/articles/06195motoneuronhyperalgesiapainspinal cord |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Mouloud Bouhadfane Attila Kaszás Balázs Rózsa Ronald M Harris-Warrick Laurent Vinay Frédéric Brocard |
spellingShingle |
Mouloud Bouhadfane Attila Kaszás Balázs Rózsa Ronald M Harris-Warrick Laurent Vinay Frédéric Brocard Sensitization of neonatal rat lumbar motoneuron by the inflammatory pain mediator bradykinin eLife motoneuron hyperalgesia pain spinal cord |
author_facet |
Mouloud Bouhadfane Attila Kaszás Balázs Rózsa Ronald M Harris-Warrick Laurent Vinay Frédéric Brocard |
author_sort |
Mouloud Bouhadfane |
title |
Sensitization of neonatal rat lumbar motoneuron by the inflammatory pain mediator bradykinin |
title_short |
Sensitization of neonatal rat lumbar motoneuron by the inflammatory pain mediator bradykinin |
title_full |
Sensitization of neonatal rat lumbar motoneuron by the inflammatory pain mediator bradykinin |
title_fullStr |
Sensitization of neonatal rat lumbar motoneuron by the inflammatory pain mediator bradykinin |
title_full_unstemmed |
Sensitization of neonatal rat lumbar motoneuron by the inflammatory pain mediator bradykinin |
title_sort |
sensitization of neonatal rat lumbar motoneuron by the inflammatory pain mediator bradykinin |
publisher |
eLife Sciences Publications Ltd |
series |
eLife |
issn |
2050-084X |
publishDate |
2015-03-01 |
description |
Bradykinin (Bk) is a potent inflammatory mediator that causes hyperalgesia. The action of Bk on the sensory system is well documented but its effects on motoneurons, the final pathway of the motor system, are unknown. By a combination of patch-clamp recordings and two-photon calcium imaging, we found that Bk strongly sensitizes spinal motoneurons. Sensitization was characterized by an increased ability to generate self-sustained spiking in response to excitatory inputs. Our pharmacological study described a dual ionic mechanism to sensitize motoneurons, including inhibition of a barium-sensitive resting K+ conductance and activation of a nonselective cationic conductance primarily mediated by Na+. Examination of the upstream signaling pathways provided evidence for postsynaptic activation of B2 receptors, G protein activation of phospholipase C, InsP3 synthesis, and calmodulin activation. This study questions the influence of motoneurons in the assessment of hyperalgesia since the withdrawal motor reflex is commonly used as a surrogate pain model. |
topic |
motoneuron hyperalgesia pain spinal cord |
url |
https://elifesciences.org/articles/06195 |
work_keys_str_mv |
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