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Updated: Jan 25, 2026

Anteromesial Temporal Lobectomy for Medically Intractable Temporal Lobe Epilepsy: An Operative Study
Published on: August 15, 2025
Increased expression of the P2X7 receptor in temporal lobe epilepsy: Animal models and clinical evidence
Penghui Song1, Jing Hu2, Xijin Liu3
1Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
Abstract:
Previous studies have indicated that the adenosine triphosphate‑sensitive homomeric P2X7 receptor (P2X7R) plays an important role and exhibits therapeutic potential in a number of brain disorders, including temporal lobe epilepsy (TLE). The aim of the present study was to assess the expression of P2X7R, glutamate (GLU) and glial fibrillary acidic protein (GFAP) in the temporal neocortex and hippocampus of rats with lithium‑pilocarpine‑induced epilepsy as well as in patients with intractable TLE. The results demonstrated that the levels of P2X7R, GLU and GFAP were significantly upregulated in rats with spontaneous recurrent seizures, whereas they were reduced in rats that were treated with brilliant blue G (BBG), a P2X7R antagonist. To the best of our knowledge, the present study is also the first to demonstrate that P2X7R expression was elevated in patients with intractable TLE. These findings suggest that P2X7R plays a key role in the development of TLE and that BBG treatment may be a promising therapeutic strategy for TLE.
Insights
The adenosine triphosphate‑sensitive homomeric P2X7 receptor (P2X7R) is upregulated in temporal lobe epilepsy (TLE). Blocking P2X7R with brilliant blue G (BBG) reduced seizures, suggesting a potential therapeutic strategy for TLE.
Area of Science:
- Neuroscience
- Pharmacology
- Epilepsy Research
Background:
- The P2X7 receptor (P2X7R) is implicated in various brain disorders, including temporal lobe epilepsy (TLE).
- Understanding P2X7R's role in TLE pathogenesis is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the expression of P2X7R, glutamate (GLU), and glial fibrillary acidic protein (GFAP) in epilepsy models and human TLE.
- To evaluate the therapeutic potential of P2X7R antagonism in TLE.
Main Methods:
- Lithium-pilocarpine-induced epilepsy model in rats.
- Assessment of P2X7R, GLU, and GFAP expression in rat temporal neocortex and hippocampus.
- Analysis of P2X7R expression in human intractable TLE patients.
- Treatment with brilliant blue G (BBG), a P2X7R antagonist.
Main Results:
- Significantly upregulated levels of P2X7R, GLU, and GFAP were observed in rats with spontaneous recurrent seizures.
- BBG treatment led to reduced levels of these markers in epileptic rats.
- Elevated P2X7R expression was confirmed in patients with intractable TLE.
Conclusions:
- P2X7R plays a critical role in the development and progression of TLE.
- BBG, as a P2X7R antagonist, shows promise as a therapeutic agent for TLE.
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