Abstract
Objective To observe the changes in the mechanical withdrawal threshold (MWT) and the proportion of GABA-immunoreactive neurons in spinal dorsal horn (SDH) of the spared nerve injury (SNI) rat model. Methods Thirty-six healthy male SD rats were randomly divided into a sham-operated group (group D, n = 18) and an SNI group (group S, n = 18). The left sciatic nerve trunk and three branches were exposed, two of which, known as tibial and the peroneal nerve, were ligated and cut off. The sural nerve was preserved to build the SNI model in group S. The left sciatic nerve trunk and three branches were only exposed in group D. MWT tests were performed on the medial and lateral sides of the rats' left hindpaw 1 day before surgery and at 7th, 14th, and 28th day after surgery. Results In group S, compared with the baseline measured 1 day before surgery, MWT on the medial and lateral sides of the rats' left hindpaw decreased significantly on the 7th, 14th, and 28th days after surgery (P < 0.05), while in group D, there was no statistically significant difference (P > 0.05). Compared with right SDH, there were not statistically significant reductions in the proportions of GABAergic neurons of left SDH on 7th and 28th day after SNI (P > 0.05); however, the proportion of GABAergic neurons in left SDH significantly decreased, compared with that in right side on 14th day after SNI (P < 0.05). On the same way, the proportions of GABAergic neurons on 7th, 14th, and 28th day after surgery were not statistically different (P > 0.05) in group D. Conclusion The SNI model could reduce the proportion of GABA-immunoreactive neurons in the rat's spinal dorsal horn on the nerve-injured side, and this change was lasting, which might be related to the transformation of the GABA-immunoreactive neurons.
Highlights
Neuropathic pain (NPP) is a chronic pain caused by nervous system damage or dysfunction and is difficult to treat, with symptoms including spontaneous pain, hyperalgesia, and allodynia
Studies [4, 5] showed that the absent GABAergic inhibition on the lamina I-III of spinal dorsal horn (SDH) is closely related to NPP, but detailed mechanism remains unknown
Yowtak [6] found that, 7 days after spinal nerve ligation (SNL) model, the amount of GABA-immunoreactive neurons in the SDH on the operated side was significantly reduced, while the GABA receptor agonists can reverse the rat’s hypersensitivity to mechanical stimulation; Inquimbert et al [7] verified the apoptosis of the spinal GABAergic neurons by using the chronic compression model (CCI) and spared nerve injury (SNI)
Summary
Neuropathic pain (NPP) is a chronic pain caused by nervous system damage or dysfunction and is difficult to treat, with symptoms including spontaneous pain, hyperalgesia, and allodynia. Model is a common and ideal model for study on NPP, with advantages of precise effect of nerve injury, good repeatability, and lasting behavioral changes and can reliably simulate the clinical symptoms of NPP [3]. Studies [4, 5] showed that the absent GABAergic inhibition on the lamina I-III of SDH is closely related to NPP, but detailed mechanism remains unknown. Yowtak [6] found that, 7 days after spinal nerve ligation (SNL) model, the amount of GABA-immunoreactive neurons in the SDH on the operated side was significantly reduced, while the GABA receptor agonists can reverse the rat’s hypersensitivity to mechanical stimulation; Inquimbert et al [7] verified the apoptosis of the spinal GABAergic neurons by using the chronic compression model (CCI) and SNI
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