ReviewMolecular pain
The etiological contribution of GABAergic plasticity to the pathogenesis of neuropathic pain.
Review in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- The efficacy and mechanisms of low-intensity transcranial ultrasound stimulation on pain: a systematic review of human and animal studies.The journal of headache and pain · 2025Pooled it
- Semaphorins and Their Role in Neuropathic Pain.Life (Basel, Switzerland) · 2026Review
- Recombinant Artemin-Fc Fusion Protein Attenuates TLR4/NF-κB-Associated Neuroinflammation and Modulates Inhibitory/Excitatory Synaptic Marker Expression After Spinal Cord Injury.CNS neuroscience & therapeutics · 2026Article
- Subcutaneous Neuromodulation Activates Central Pain-Suppression Pathways for Analgesia.CNS neuroscience & therapeutics · 2026Article
- Astrocyte store-operated calcium entry is required for centrally mediated neuropathic pain.Pain reports · 2026Article
- Acute pain transfusion reaction in a patient with thalassemia: In-depth characterization of short- and long-term phenotypes.Transfusion · 2026Article
- Applications of micro/nano drug delivery systems in cancer pain management.Bioactive materials · 2026Review
- Electroacupuncture Attenuates Cyclophosphamide-Induced Bladder Pain by Restoring Autophagy in Spinal Inhibitory Interneurons.ACS omega · 2026Article
- Targeting NMDA receptors in pain management: therapeutic innovations through piracetam repurposing.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Review
- Article
- Transcriptomic and molecular evidence for baclofen-associated modulation of inhibitory synaptic and neuroinflammatory pathways in diabetic neuropathic pain.Frontiers in pharmacology · 2026Article
- Curcumin reduces pain after spinal cord injury in rats by decreasing oxidative stress and increasing GABAA receptor and GAD65 levels.Scientific reports · 2025Article
- Neuroplasticity in chronic pain: insights into diagnosis and treatment.The Korean journal of pain · 2025Article
- Modulating neuroplasticity for chronic pain relief: noninvasive neuromodulation as a promising approach.Experimental & molecular medicine · 2025Review
- Distinct Roles of Astrocytes and GABAergic Neurons in the Paraventricular Thalamic Nucleus in Modulating Diabetic Neuropathic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Anti-Hyperalgesic Effect of Isopulegol Involves GABA and NMDA Receptors in a Paclitaxel-Induced Neuropathic Pain Model.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Modulation of pain sensitivity by Ascl1- and Lhx6-dependent GABAergic neuronal function in streptozotocin diabetic mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Discovery of Novel Pain Regulators Through Integration of Cross-Species High-Throughput Data.CNS neuroscience & therapeutics · 2025Article
- N-Demethylsinomenine Relieves Neuropathic Pain in Male Mice Mainly via Regulating α2-Subtype GABACNS neuroscience & therapeutics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain developing after peripheral or central nerve injury is the result of pathological changes generated through complex mechanisms. Disruption in the homeostasis of excitatory and inhibitory neurons within the central nervous system is a crucial factor in the formation of hyperalgesia or allodynia occurring with neuropathic pain. The central GABAergic pathway has received attention for its extensive distribution and function in neural circuits, including the generation and development of neuropathic pain. GABAergic inhibitory changes that occur in the interneurons along descending modulatory and nociceptive pathways in the central nervous system are believed to generate neuronal plasticity, such as synaptic plasticity or functional plasticity of the related genes or proteins, that is the foundation of persistent neuropathic pain. The primary GABAergic plasticity observed in neuropathic pain includes GABAergic synapse homo- and heterosynaptic plasticity, decreased synthesis of GABA, down-expression of glutamic acid decarboxylase and GABA transporter, abnormal expression of NKCC1 or KCC2, and disturbed function of GABA receptors. In this review, we describe possible mechanisms associated with GABAergic plasticity, such as central sensitization and GABAergic interneuron apoptosis, and the epigenetic etiologies of GABAergic plasticity in neuropathic pain. Moreover, we summarize potential therapeutic targets of GABAergic plasticity that may allow for successful relief of hyperalgesia from nerve injury. Finally, we compare the effects of the GABAergic system in neuropathic pain to other types of chronic pain to understand the contribution of GABAergic plasticity to neuropathic pain.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.