AbstractAimsLow back pain and sciatica after disc herniation may be caused by mechanical compression of the nerve roots, but also by the release of pro-inflammatory agents including growth factors from the nucleus pulposus (NP).MethodsHere, in an animal model mimicking the clinical situation following disc herniation, CLIA protein analyses, extracellular single-cell recordings in the spinal dorsal horn and qPCR were performed to examine the nociceptive signaling due to disc herniation.Results The present data demonstrated that EREG may be released from NP - and that administration of EREG onto the spinal dorsal nerve roots increased spontaneous activity in nociceptive neurons. An up-regulation of EGFR and HER4 in the dorsal horn as well as an up-regulation of HER3 in the DRG were demonstrated after application of NP onto the dorsal nerve roots.ConclusionOur findings suggest that EREG and signaling through its receptors may be involved in pain hypersensitivity and other sensory abnormalities after disc herniation.
Scandinavian Journal of Pain – de Gruyter
Published: Jul 1, 2016
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