Involvement between social defeat stress and pain-related behavior in a rat lumbar disk herniation model
- PDF / 2,826,433 Bytes
- 10 Pages / 595.276 x 790.866 pts Page_size
- 25 Downloads / 184 Views
ORIGINAL ARTICLE
Involvement between social defeat stress and pain‑related behavior in a rat lumbar disk herniation model Shota Yomogida1 · Miho Sekiguchi1 · Shin‑ichi Konno1 Received: 5 January 2020 / Revised: 7 June 2020 / Accepted: 9 July 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Introduction Psychological and social factors are involved in the disability and chronicity of pain. Our study aim was to investigate whether social defeat stress (SDS) as a psychophysical stress affected mechanical withdrawal thresholds in the lumbar disk herniation (LDH) rat model. Changes in microglia and astrocytes, which play important roles in neuropathic pain states, were also investigated. Materials and methods For the LDH model, nucleus pulposus (NP) was applied to the L5 dorsal root ganglion (DRG) in adult female Sprague–Dawley rats. SDS was performed 15 min daily for 8 days. Mechanical withdrawal thresholds were measured, and immunoreactive cells of glial fibrillary acidic protein (GFAP) and ionized calcium-binding adaptor molecule-1 (Iba-1), which were used as markers of microglia, satellite glial cells, and astrocytes, were assessed in the DRG, spinal cord (SC), and ventrolateral periaqueductal gray matter (VLPAG). Results Mechanical withdrawal thresholds decreased in the NP group for 21 days and for 35 days in the NP + SDS group. Expression of GFAP and Iba-1 in the DRG and SC increased up to day 21 in the NP and NP + SDS groups. In the sham + SDS and NP + SDS groups, expression of GFAP in the VLPAG decreased until day 35. Conclusion SDS prolongs mechanical allodynia induced by NP. Changes of GFAP expression in the VLPAG were associated with mechanical allodynia of the NP + SDS group during the late phase. These results suggest that psychological chronic stress might delay recovery from mechanical allodynia induced by the LDH model. Keywords Lumbar disk herniation · Neuropathic pain · Social defeat stress · Periaqueductal gray matter · Glial fibrillary acidic protein
Introduction Lumbar disk herniation (LDH), which is one of the most common diseases responsible for low back pain and radiculopathy, is caused by both mechanical compression and inflammation associated with chemical factors [1, 14, 22–24, 26, 30, 32, 36, 37]. Previous studies have demonstrated that the size of the herniated disk does not correspond to the clinical symptoms [5, 6]. In addition, in vivo studies have shown that chemical factors found in the intervertebral disk induce neuropathic pain [14, 24, 36, 38]. Moreover, several animal models have shown that the expression of proinflammatory cytokines and glial cells in the spinal cord * Miho Sekiguchi miho‑[email protected] 1
Department of Orthopaedic Surgery, Fukushima Medical University School of Medicine, Fukushima, Japan
(SC) and dorsal root ganglion (DRG) are implicated in the neuropathic pain states [11, 35, 47, 51]. Based on these findings, chemical factors are now being focused on as pharmacological targets. However, some of these recommended pharmacological
Data Loading...
