Sensitization of neonatal rat lumbar motoneuron by the inflammatory pain mediator bradykinin

ELife
Mouloud BouhadfaneFrédéric Brocard

Abstract

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.

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Citations

Dec 5, 2015·The Journal of Physiology·S MandadiP J Whelan
Mar 26, 2016·Frontiers in Neuroscience·Giandomenico D'AlessandroPietro Cortelli
Aug 14, 2020·Molecular Pain·Muhammad Saad YousufBradley J Kerr
Sep 21, 2021·Experimental and Therapeutic Medicine·Xin MengJingwei Chen

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Software Mentioned

MES
Clampfit
Femtonics
Clampex
Matlab
GraphPad

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