SCIENCE@home

The impact of guanethidine-induced sympathectomy on satellite glial cell activation in a rat model of neuropathic pain.

Xicun Han,Xiaohua Jiang,Yabin Liu,Guowu Chen

Published 2025 in Neuroscience Letters

ABSTRACT

The involvement of satellite glial cells (SGCs) in neuropathic pain has been well-established; however, it remains unclear whether the sprouted sympathetic fibers within the dorsal root ganglion (DRG) after peripheral nerve injury affect the activation of SGCs. A rat model of neuropathic pain induced by spinal nerve ligation injury (SNL) was established. The mechanical withdrawal threshold (MWT) was evaluated using the von Frey test on postoperative days (POD) 1, 3, 7, and 14 to quantify mechanical allodynia. Immunofluorescence staining was performed to detect the expression of glial fibrillary acidic protein (GFAP, a marker for activated SGCs), tyrosine hydroxylase (TH, a marker for sympathetic nerve fibers), and α2-adrenergic receptor (α2-AR) in the ipsilateral DRG. Reversible sympathectomy was achieved by means of a single high-dose intraperitoneal injection of guanethidine (Gua). Western blotting(WB) was used to assess the effect of sympathectomy on GFAP expression in the DRG of SNL rats. After spinal nerve injury, the MWT of the ipsilateral hindlimb in rats decreased rapidly. Immunofluorescence results confirmed that the expression levels of GFAP and TH in the ipsilateral DRG of SNL rats gradually increased along with the development of mechanical allodynia. Notably, the co-expression of α2-AR and GFAP in the DRG gradually increased after SNL, suggesting that the newly formed noradrenergic-SGCs signaling within the DRG was involved in the initiation and maintenance of neuropathic pain. On 14 days post-SNL, Gua-induced sympathectomy significantly alleviated mechanical allodynia in rats and remarkably inhibited GFAP expression in the ipsilateral DRG. We concluded that in the rat model of neuropathic pain induced by SNL, the sprouted sympathetic fibers within the DRG may also participate in the maintenance of neuropathic pain by regulating the activation of SGCs.

PUBLICATION RECORD

CITATION MAP

EXTRACTION MAP

CLAIMS

  • No claims are published for this paper.

CONCEPTS

  • No concepts are published for this paper.

REFERENCES

Showing 1-35 of 35 references · Page 1 of 1

CITED BY

  • No citing papers are available for this paper.

Showing 0-0 of 0 citing papers · Page 1 of 1