Change in GABA receptor-activated current in dorsal root ganglion neurons freshly isolated from rats with neuropathic pain
10.3760/cma.j.issn.0254-1416.2011.01.017
- VernacularTitle:神经病理性痛大鼠背根神经节神经元γ氨基丁酸激活电流的改变
- Author:
Ran RAN
;
Shanglong YAO
;
Kaifeng YU
;
Qun WANG
;
Qingxiu WANG
;
Junfeng GU
;
Gang TIAN
- Publication Type:Journal Article
- Keywords:
Gamma-aminobutyric acid;
Ganglia,spinal;
Neuralgia
- From:
Chinese Journal of Anesthesiology
2011;31(1):55-58
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the change in GABA receptor-activated current in dorsal root ganglion (DRG) neurons in rats with neuropathic pain. Methods Twenty adult SD rats of both sexes weighing 100-150 g were randomly divided into 2 gorups: sham operation group (group S, n = 5) and neuropathic pain group (group NP, n= 15). Neuropathic pain was induced by ligation of right L5 spinal nerve. The animals were sacrificed at 5 days after operation. The L5 DRG( neurons in group NP and L3-5 DRG neurons in group S were immediately isolated. Whole-cellpatch- clamp technique was used. The extracellular solution contained GABA 100μmol/L.The frequency and amplitude of the GABA-activated current in DRG neurons and the changes in action potential (threshold potential, rheobase and overshoot) and resting potential before and after GABA administration were recorded. Results GABA 100μmol/L induced rapid inactivation of inward current in most neurons. Compared with the baseline before application of GABA, in group S GABA induced depolarization,increased resting potential and decreased amplitude and rheobase of action potential in large and medium DRG neurons, while in group NP GABA increased resting potential but induced no significant change in threshold potential and rheobase and overshoot of action potential. The frequency and amplitude of GABA-activated current and the degree of change in resting potential and rheobase and overshoot of action potential were significantly lower in group NP than in group S.Spontaneous discharge occurred in small DRG neurons in both groups. No GABA-activated current was observed in all DRG neurons with spontaneous discharge. Conclusions Neuropathic pain is induced by decreasing GABA-mediated inhibition signals in large and medium DRG neurons leading to increased excitability of neurons.
