ArticleGene expression2015
Comprehensive analysis of the GABAergic system gene expression profile in the anterior cingulate cortex of mice with Paclitaxel-induced neuropathic pain.
Article in Gene expression, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 43 citations in OpenAlex.
- 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
- Decoding chronic pain: the glutamate-GABA tug of war in the cerebral cortex.Frontiers in molecular neuroscience · 2025Review
- Current understanding of the molecular mechanisms of chemotherapy-induced peripheral neuropathy.Frontiers in molecular neuroscience · 2024Review
- Muscimol inhibits plasma membrane rupture and ninjurin-1 oligomerization during pyroptosis.Communications biology · 2023Article
- Anxiolytic effect of GABAergic neurons in the anterior cingulate cortex in a rat model of chronic inflammatory pain.Molecular brain · 2021Article
- Acupuncture for Paclitaxel-Induced Peripheral Neuropathy: A Review of Clinical and Basic Studies.Journal of pain research · 2021Review
- The Medial Prefrontal Cortex as a Central Hub for Mental Comorbidities Associated with Chronic Pain.International journal of molecular sciences · 2020Review
- GABAergic cell transplants in the anterior cingulate cortex reduce neuropathic pain aversiveness.Brain : a journal of neurology · 2019Article
- Von Economo Neurons and Fork Cells: A Neurochemical Signature Linked to Monoaminergic Function.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
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- Paclitaxel Causes Electrophysiological Changes in the Anterior Cingulate Cortex via Modulation of the γ-Aminobutyric Acid-ergic System.Medical principles and practice : international journal of the Kuwait University, Health Science CentreArticle
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1 author at 1 institution in 1 country.
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Abstract
The supraspinal pathophysiology of the painful neuropathy induced by paclitaxel, a chemotherapeutic agent, is not well understood. The γ-aminobutyric acid (GABA) neurotransmitter system has been implicated in the pathogenesis of neuropathic pain. Gene expression of GABAergic system molecules was examined in the anterior cingulate cortex (ACC) of mice brains, by real-time PCR, during paclitaxel-induced neuropathic pain, because this area is involved in pain perception and modulation that might contribute to neuropathic pain. Paclitaxel treatment resulted in thermal hyperalgesia and in increased GABA transporter-1 (GAT-1) mRNA expression, but not that of other GABA transporters or GABA(A) ergic enzymes in the ACC compared to vehicle treatment. Among the 18 GABA(A) receptor subunits analyzed, only β2, β3, δ, and γ2 had increased mRNA levels, and for the receptor subunit, only GABA(B2) had increased mRNA levels in the ACC of paclitaxel-treated mice, whereas the rest of the GABA receptor subunits were not altered. The mRNA expression of GABAA receptor subunits α6, θ, π, ρ1, ρ2, and ρ3 were not detected in the ACC. In conclusion, these data show that during paclitaxel-induced neuropathic pain there is significant increase in GAT-1 expression in the ACC. GAT-1 is the main transporter of GABA from the synapse, and thus its increased expression possibly results in less GABA at the synapse and dysregulation of the GABAergic system. GAT-1 is a potential therapeutic target for managing paclitaxel-induced neuropathic pain.
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