Effects of niflumic acid on γ‑aminobutyric acid‑induced currents in isolated dorsal root ganglion neurons of neuropathic pain rats

Wang,Li‑Jie; Wang,Yang; Chen,Meng‑Jie; Tian,Zhen‑Pu; Lu,Bi‑Han; Mao,Ke‑Tao; Zhang,Liang; Zhao,Lei; Shan,Li‑Ya; Li,Li; Si,Jun‑Qiang

doi:10.3892/etm.2017.4666

Effects of niflumic acid on γ‑aminobutyric acid‑induced currents in isolated dorsal root ganglion neurons of neuropathic pain rats

Authors:
- Li‑Jie Wang
- Yang Wang
- Meng‑Jie Chen
- Zhen‑Pu Tian
- Bi‑Han Lu
- Ke‑Tao Mao
- Liang Zhang
- Lei Zhao
- Li‑Ya Shan
- Li Li
- Jun‑Qiang Si
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Affiliations: Department of Physiology, Shihezi University Medical College, Shihezi, Xinjiang 832002, P.R. China
Published online on: June 26, 2017 https://doi.org/10.3892/etm.2017.4666
Pages: 1373-1380
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Niflumic acid (NFA) is a type of non‑steroidal anti‑inflammatory drug. Neuropathic pain is caused by a decrease in presynaptic inhibition mediated by γ‑aminobutyric acid (GABA). In the present study, a whole‑cell patch‑clamp technique and intracellular recording were used to assess the effect of NFA on GABA‑induced inward current in dorsal root ganglion (DRG) neurons of a chronic constriction injury (CCI) model. It was observed that 1‑1,000 µmol/l GABA induced a concentration‑dependent inward current in DRG neurons. Compared with pseudo‑operated rats, the thermal withdrawal latency (TWL) of CCI rats significantly decreased (P<0.01); however, the TWLs of each NFA group (50 and 300 µmol/l) were significantly longer than that of the CCI group (P<0.01). In the CCI group, the response evoked by GABA (10‑6‑10‑3 mol/l) was reduced in a concentration dependent manner compared with a normal control group (P<0.01), and the current amplitudes of CCI rats activated by the same concentrations of GABA (10‑6‑10‑3 mol/l) were significantly decreased compared with the control group (P<0.05). The inward currents activated by 100 µmol/l GABA were suppressed by treatment with 1, 10 and 100 µmol/l NFA (5.32±3.51, 33.8±5.20, and 52.2±6.32%, respectively; P<0.05). The inverse potentials of GABA‑induced currents were 9.87±1.32 and 9.64±1.24 mV with and without NFA, respectively (P<0.05). Pre‑treatment with NFA exerted a strong inhibitory effect on the peak value of GABA‑induced current, and the GABA‑induced response was inhibited by the same concentrations of NFA (1, 10 and 100 µmol/l) in the control and CCI groups (P<0.05). The results suggest that NFA reduced the primary afferent depolarization (PAD) associated with neuropathic pain and mediated by the GABAA receptor. NFA may regulate neuropathic pain by inhibiting dorsal root reflexes, which are triggered PAD.

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