Extracellular signal-regulated kinases mediate melittin-induced hypersensitivity of spinal neurons to chemical and thermal but not mechanical stimuli
Abstract
Subcutaneous melittin injection causes central plasticity at the spinal level in wide-dynamic-range (WDR) neurons, which are hypersensitive to various nociceptive stimuli. Previous behavioral studies demonstrated that the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase 1/2(ERK1/2), p38 MAPK, and c-Jun N-terminal kinase are involved in both peripheral and spinal processing of melittin-induced nociception and hypersensitivity. Yet the functional roles of the three MAPKs vary among different stimulus modalities, and must be further studied at the cellular level in vivo. In this report, extracellular single unit recordings were performed to investigate whether activation of ERK1/2 in the primary injury site of melittin is essential to the establishment of a spinally sensitized state. Localized peripheral administration of a single dose of the MEK inhibitor U0126 (1 μg/10 μl) significantly suppressed neuronal hyper-responsiveness to thermal stimulus and chemical (melittin)-induced tonic firing of WDR neurons after full establishment of a spinally sensitized state. However, U0126 failed to affect mechanical hypersensitivity to both noxious and non-noxious stimuli. Melittin-induced enhancement of therma...Continue Reading
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