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The P2X7 Hypothesis of Central Post-Stroke Pain: Modulations of P2X7 Receptors Influence Central Post-Stroke Pain Regarding Behaviors, Electrophysiological Activity, and Molecular Expression in Mice
Version 1
: Received: 10 February 2024 / Approved: 12 February 2024 / Online: 12 February 2024 (13:11:57 CET)
How to cite:
Huang, A. C.-W.; Shih, H. C.; Shyu, B. C. The P2X7 Hypothesis of Central Post-Stroke Pain: Modulations of P2X7 Receptors Influence Central Post-Stroke Pain Regarding Behaviors, Electrophysiological Activity, and Molecular Expression in Mice. Preprints2024, 2024020661. https://doi.org/10.20944/preprints202402.0661.v1
Huang, A. C.-W.; Shih, H. C.; Shyu, B. C. The P2X7 Hypothesis of Central Post-Stroke Pain: Modulations of P2X7 Receptors Influence Central Post-Stroke Pain Regarding Behaviors, Electrophysiological Activity, and Molecular Expression in Mice. Preprints 2024, 2024020661. https://doi.org/10.20944/preprints202402.0661.v1
Huang, A. C.-W.; Shih, H. C.; Shyu, B. C. The P2X7 Hypothesis of Central Post-Stroke Pain: Modulations of P2X7 Receptors Influence Central Post-Stroke Pain Regarding Behaviors, Electrophysiological Activity, and Molecular Expression in Mice. Preprints2024, 2024020661. https://doi.org/10.20944/preprints202402.0661.v1
APA Style
Huang, A. C. W., Shih, H. C., & Shyu, B. C. (2024). The P2X7 Hypothesis of Central Post-Stroke Pain: Modulations of P2X7 Receptors Influence Central Post-Stroke Pain Regarding Behaviors, Electrophysiological Activity, and Molecular Expression in Mice. Preprints. https://doi.org/10.20944/preprints202402.0661.v1
Chicago/Turabian Style
Huang, A. C., Hsi Chien Shih and Bai Chuang Shyu. 2024 "The P2X7 Hypothesis of Central Post-Stroke Pain: Modulations of P2X7 Receptors Influence Central Post-Stroke Pain Regarding Behaviors, Electrophysiological Activity, and Molecular Expression in Mice" Preprints. https://doi.org/10.20944/preprints202402.0661.v1
Abstract
Whether and how P2X7 receptor knockout (KO) modulates central post-stroke pain (CPSP) induced by lesions of the ventrobasal complex (VBC) of the thalamus regarding behavioral, molecular, and electrical recording parameters remains unclear. Following the experimental protocols of a rat hemorrhage CPSP model, the VBC of the thalamus of wild-type and P2X7 receptor KO mice was injected with 10 mU/0.2 μl type IV collagenase to produce an animal model of stroke-like thalamic hemorrhage. Behavioral data showed that the CPSP group induced thermal and mechanical pain, while the P2X7 receptor KO group showed reduced thermal and mechanical pain behaviors. Molecular assessments revealed that the CPSP group had lower expression of NeuN and KCC2 and higher expression of GFAP, IBA1, and BDNF. The P2X7 KO group showed lower expression of GFAP, IBA1, and BDNF and higher expression of KCC2 than the CPSP group. The expression of NKCC1, GABAa receptor, and TrkB did not differ significantly between the control, CPSP, and P2X7 receptor KO groups. Muscimol application increased multiunit numbers and [Cl-] influx in the membrane in the CPSP group, while P2X7 receptor KO reduced multiunit activity and [Cl-] outflux. P2X4 receptor expression was significantly decreased in the 100 kb but not the 50 kb site in the P2X7 receptor KO group. Altogether, the P2X7 hypothesis of CPSP was proposed, wherein P2X7 receptor KO changed the CPSP pain behavior, numbers of astrocytes and microglia, CSD amplitude of the anterior cingulate cortex and the medial dorsal thalamus, BDNF and KCC2 expression, [Cl-], and P2X4 activation in 100 kb with P2X7 receptors. The present findings have implications for the clinical treatment of CPSP symptoms.
Keywords
CPSP; P2X7 receptor; the P2X7 hypothesis of central post-stroke pain; stroke hemorrhage; mice
Subject
Medicine and Pharmacology, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
