Expression of LC3 and Beclin 1 in the spinal dorsal horn following spinal nerve ligation-induced neuropathic pain.

Impaired spinal GABAergic inhibitory function is known to be pivotal in neuropathic pain (NPP). At present, data concerning time-dependent alterations in cell type and cell death in the spinal dorsal horn are highly controversial, likely related to the experimental NPP model used. In this study, we examined the expression of autophagy using a L5 spinal nerve ligation (SNL)-induced neuropathic pain rat model. Following ligation of the spinal nerve, neuropathic pain behavior, such as mechanical allodynia, was induced rapidly and maintained for 14 days. After testing for mechanical allodynia, we assessed the changes in expression of LC3 and Beclin 1 in the spinal cord following SNL. Immunohistochemical analysis showed that the levels of LC3 and Beclin 1 protein in the ipsilateral L5 spinal dorsal horn were significantly elevated on day 14 following SNL. Double immunohistochemical analysis further confirmed increases in LC3 and Beclin 1 in mostly neurons and a few astrocytes following SNL. LC3 and Beclin 1 expressions were upregulated in GABAergic interneurons of spinal dorsal horn after SNL, while the loss of GABAergic interneurons did not change significantly. Our results suggest that autophagic disruption in GABAergic interneurons and astrocytes following peripheral nerve injury might be involved in the induction and maintenance of neuropathic pain.