Changes in expression of gamma-aminobutyric acid receptor subunit genes in dorsal root ganglia in a mouse model of neuropathic pain

Abstract

Objective To evaluate the changes in the expression of gamma-aminobutyric acid (GABA) receptor subunit genes in the dorsal root ganglia (DRG) in a mouse model of neuropathic pain. Methods Experiment Ⅰ Twenty-four male C57BL6 mice, aged 8 weeks, weighing 25-30 g, were divided into sham operation group (group Sham, n=12) and neuropathic pain group (group NP, n=12) by using a random number table method.Neuropathic pain was produced by bilateral L4 spinal nerve ligation in anesthetized mice in group NP.The mechanical pain threshold of bilateral hindpaws was measured at 1 day before establishing the model and 7 days after establishing the model.Mice were then sacrificed and DRGs of the bilateral L4 were removed to perform transcriptome sequencing and to analyze the expression of GABA receptor subunit genes.Experiment Ⅱ Twenty-four male C57BL6 mice, aged 8 weeks, weighing 25-30 g, were studied.Neuropathic pain was produced by the left L4 spinal nerve ligation in anesthetized mice.Six mice were selected at 1 day before establishing the model and 3, 7 and 14 days after establishing the model, and the mechanical pain threshold of the left hindpaw was measured.Mice were then sacrificed and DRGs of the left L4 were removed to verify the expression of differentially expressed GABA receptor subunit genes described in experiment Ⅰby quantitative real-time polymerase chain reaction. Results Experiment Ⅰ Compared with group Sham, the mechanical pain threshold was significantly increased, the expression of Gabra1, Gabra2, Gabrb3, Gabrg2, Gabbr1 and Gabbr2 in DRGs was down-regulated, and the expression of Gabrg1 in DRGs was up-regulated at 7 days after establishing the model in group NP (P 0.05). Conclusion The expression of GABA receptor subunit genes Gabra1, Gabra2, Gabrb3, Gabrg2, Gabbr1 and Gabbr2 in DRGs is down-regulated, and the expression of Gabrg1 in DRGs is up-regulated in a mouse model of neuropathic pain. Key words: Neuralgia; Receptors, GABA; Ganglia, spinal