The University of Alabama
  • Log In
    New user? Click here to register. Have you forgotten your password?
  • About the repository
  • Open Access
  • Research Data Services
  • University Libraries
  • Login
University Libraries
    Communities & Collections
    Explore
  1. Home
  2. Browse by Author

Browsing by Author "Lee, Sunyeul"

Now showing 1 - 1 of 1
Results Per Page
Sort Options
  • Loading...
    Thumbnail Image
    Item
    Endoplasmic reticulum stress impairment in the spinal dorsal horn of a neuropathic pain model
    (Nature Portfolio, 2015) Zhang, Enji; Yi, Min-Hee; Shin, Nara; Baek, Hyunjung; Kim, Sena; Kim, Eunjee; Kwon, Kisang; Lee, Sunyeul; Kim, Hyun-Woo; Bae, Yong Chul; Kim, Yonghyun; Kwon, O. -Yu; Lee, Won Hyung; Kim, Dong Woon; Chungnam National University; Chungnam National University Hospital; Kyungpook National University; Yanbian University; University of Alabama Tuscaloosa
    Endoplasmic reticulum (ER) stress has been implicated in neurodegenerative diseases, but its role in neuropathic pain remains unclear. In this study, we examined the ER stress and the unfolded protein response (UPR) activation in a L5 spinal nerve ligation (SNL)-induced rat neuropathic pain model. SNL-induced neuropathic pain was assessed behaviorally using the CatWalk system, and histologically with microglial activation in the dorsal spinal horn. L5 SNL induced BIP upregulation in the neuron of superficial laminae of dorsal spinal horn. It also increased the level of ATF6 and intracellular localization into the nuclei in the neurons. Moreover, spliced XBP1 was also markedly elevated in the ipsilateral spinal dorsal horn. The PERK-elF2 pathway was activated in astrocytes of the spinal dorsal horn in the SNL model. In addition, electron microscopy revealed the presence of swollen cisternae in the dorsal spinal cord after SNL. Additionally, inhibition of the ATF6 pathway by intrathecal treatment with ATF6 siRNA reduced pain behaviors and BIP expression in the dorsal horn. The results suggest that ER stress might be involved in the induction and maintenance of neuropathic pain. Furthermore, a disturbance in UPR signaling may render the spinal neurons vulnerable to peripheral nerve injury or neuropathic pain stimuli.

Fulfill funder &
journal policies

Increase your
reach and impact

Preserve your works

University Libraries
Tel: +1205-348-8647ir@ua.edu
PrivacyDisclaimerAccessibilityCopyright © 2024