ArticleMedical principles and practice : international journal of the Kuwait University, Health Science Centre
Paclitaxel Causes Electrophysiological Changes in the Anterior Cingulate Cortex via Modulation of the γ-Aminobutyric Acid-ergic System.
Article in Medical principles and practice : international journal of the Kuwait University, Health Science Centre. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Mechanism-based management of taxane-induced neuropathic pain in breast cancer survivors: a critical review.Frontiers in pain research (Lausanne, Switzerland) · 2026Review
- A newly designed GABA-AT inactivator, (bioRxiv : the preprint server for biology · 2025Article
- Efficacy of GABA aminotransferase inactivator OV329 in models of neuropathic and inflammatory pain without tolerance or addiction.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Paclitaxel-induced cognitive impairment: mechanistic insights.Frontiers in pharmacology · 2025Review
- Transcranial magnetic stimulation measures of corticospinal excitability in Black and Hispanic/Latino people with painful peripheral neuropathy.Frontiers in human neuroscience · 2025Article
- Decoding chronic pain: the glutamate-GABA tug of war in the cerebral cortex.Frontiers in molecular neuroscience · 2025Review
- Licofelone, a Dual COX/LOX Inhibitor, Ameliorates Paclitaxel-Induced Mechanical Allodynia in Rats in a Cannabinoid Receptor-Dependent Manner.Biomedicines · 2024Article
- Feasibility of trancutaneous auricular vagus nerve stimulation in Black and Hispanic/Latino people with peripheral neuropathy.Frontiers in pain research (Lausanne, Switzerland) · 2024Article
- Current understanding of the molecular mechanisms of chemotherapy-induced peripheral neuropathy.Frontiers in molecular neuroscience · 2024Review
- Paclitaxel triggers molecular and cellular changes in the choroid plexus.Frontiers in pain research (Lausanne, Switzerland) · 2024Article
- Excitatory and inhibitory neuronal signaling in inflammatory and diabetic neuropathic pain.Molecular medicine (Cambridge, Mass.) · 2023Review
- [6]-Shogaol Attenuates Oxaliplatin-Induced Allodynia through Serotonergic Receptors and GABA in the Spinal Cord in Mice.Pharmaceuticals (Basel, Switzerland) · 2022Article
- GABACurrent topics in behavioral neurosciences · 2022Review
- Anxiolytic effect of GABAergic neurons in the anterior cingulate cortex in a rat model of chronic inflammatory pain.Molecular brain · 2021Article
- Review of the Role of the Brain in Chemotherapy-Induced Peripheral Neuropathy.Frontiers in molecular biosciences · 2021Review
- The Medial Prefrontal Cortex as a Central Hub for Mental Comorbidities Associated with Chronic Pain.International journal of molecular sciences · 2020Review
- Enhancing KCNQ Channel Activity Improves Neurobehavioral Recovery after Spinal Cord Injury.The Journal of pharmacology and experimental therapeutics · 2020Article
- GABAergic cell transplants in the anterior cingulate cortex reduce neuropathic pain aversiveness.Brain : a journal of neurology · 2019Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe aim of this study was to elucidate any electrophysiological changes that may contribute to the development of neuropathic pain during treatment with the anticancer drug paclitaxel, particularly in the γ-aminobutyric acid (GABA) system. MATERIALS AND
methodsOne hundred and eight Sprague-Dawley rats were used (untreated control: 43; vehicle-treated: 21, and paclitaxel-treated: 44). Paclitaxel (8 mg/kg) was administered intraperitoneally on 2 alternate days to induce mechanical allodynia. The rats were sacrificed 7 days after treatment to obtain slices of the anterior cingulate cortex (ACC), a brain region involved in the central processing of pain. Field excitatory postsynaptic potentials (fEPSPs) were recorded in layer II/III of ACC slices, and stimulus-response curves were constructed. The observed effects were pharmacologically characterized by bath application of GABA and appropriate drugs to the slices.
resultsThe paclitaxel-treated rats developed mechanical allodynia (i.e. reduced withdrawal threshold to mechanical stimuli). Slices from paclitaxel-treated rats produced a significantly higher maximal response (Emax) than those from untreated rats (p < 0.001). Bath application of GABA (0.4 µM) reversed this effect and returned the excitability to a level similar to control. Pretreatment of the slices with the GABAB receptor blocker CGP 55845 (50 µM) increased Emax in slices from untreated rats (p < 0.01) but not from paclitaxel-treated rats.
conclusionIn this study, there was a GABA deficit in paclitaxel-treated rats compared to untreated ones. Such a deficit could contribute to the pathophysiology of paclitaxel-induced neuropathic pain (PINP). Thus, the GABAergic system might be a potential therapeutic target for managing PINP.
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