ArticleExperimental and therapeutic medicine2017
Effects of niflumic acid on γ-aminobutyric acid-induced currents in isolated dorsal root ganglion neurons of neuropathic pain rats.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Pleiotropic Effects of the NSAID Fenamates on Chloride Channels: Opportunity for Ion Channelopathies?Pharmacology research & perspectives · 2025Review
- Positive interaction between GPER and β-alanine in the dorsal root ganglion uncovers potential mechanisms: mediating continuous neuronal sensitization and neuroinflammation responses in neuropathic pain.Journal of neuroinflammation · 2022Article
- The Role of TMEM16A/ERK/NK-1 Signaling in Dorsal Root Ganglia Neurons in the Development of Neuropathic Pain Induced by Spared Nerve Injury (SNI).Molecular neurobiology · 2021Article
- Antinociceptive effect of Lonchocarpus araripensis lectin: activation of L-arginine/NO/cGMP/KInflammopharmacology · 2020Article
- Expression and effect of sodium-potassium-chloride cotransporter on dorsal root ganglion neurons in a rat model of chronic constriction injury.Neural regeneration research · 2020Article
- Mechanism of persistent hyperalgesia in neuropathic pain caused by chronic constriction injury.Neural regeneration research · 2019Article
- 17β-Estradiol Attenuates Neuropathic Pain Caused by Spared Nerve Injury by Upregulating CIC-3 in the Dorsal Root Ganglion of Ovariectomized Rats.Frontiers in neuroscience · 2019Article
- Human Dorsal Root Ganglia.Frontiers in cellular neuroscience · 2019Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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
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