Research ExplorerPublicationsMicroglial P2X4 receptors are essential for spinal neurons h...

Microglial P2X4 receptors are essential for spinal neurons hyperexcitability and tactile allodynia in male and female neuropathic mice

Standard

Microglial P2X4 receptors are essential for spinal neurons hyperexcitability and tactile allodynia in male and female neuropathic mice. / Gilabert, Damien; Duveau, Alexia; Carracedo, Sara; Linck, Nathalie; Langla, Adeline; Muramatsu, Rieko; Koch-Nolte, Friedrich; Rassendren, François; Grutter, Thomas; Fossat, Pascal; Boué-Grabot, Eric; Ulmann, Lauriane.

In: ISCIENCE, Vol. 26, No. 11, 17.11.2023, p. 108110.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Gilabert, D, Duveau, A, Carracedo, S, Linck, N, Langla, A, Muramatsu, R, Koch-Nolte, F, Rassendren, F, Grutter, T, Fossat, P, Boué-Grabot, E & Ulmann, L 2023, 'Microglial P2X4 receptors are essential for spinal neurons hyperexcitability and tactile allodynia in male and female neuropathic mice', ISCIENCE, vol. 26, no. 11, pp. 108110. https://doi.org/10.1016/j.isci.2023.108110

APA

Gilabert, D., Duveau, A., Carracedo, S., Linck, N., Langla, A., Muramatsu, R., Koch-Nolte, F., Rassendren, F., Grutter, T., Fossat, P., Boué-Grabot, E., & Ulmann, L. (2023). Microglial P2X4 receptors are essential for spinal neurons hyperexcitability and tactile allodynia in male and female neuropathic mice. ISCIENCE, 26(11), 108110. https://doi.org/10.1016/j.isci.2023.108110

Vancouver

Gilabert D, Duveau A, Carracedo S, Linck N, Langla A, Muramatsu R et al. Microglial P2X4 receptors are essential for spinal neurons hyperexcitability and tactile allodynia in male and female neuropathic mice. ISCIENCE. 2023 Nov 17;26(11):108110. https://doi.org/10.1016/j.isci.2023.108110

Bibtex

@article{c8235c281bb9487dbe12e8665fa52f70,
title = "Microglial P2X4 receptors are essential for spinal neurons hyperexcitability and tactile allodynia in male and female neuropathic mice",
abstract = "In neuropathic pain, recent evidence has highlighted a sex-dependent role of the P2X4 receptor in spinal microglia in the development of tactile allodynia following nerve injury. Here, using internalization-defective P2X4mCherryIN knockin mice (P2X4KI), we demonstrate that increased cell surface expression of P2X4 induces hypersensitivity to mechanical stimulations and hyperexcitability in spinal cord neurons of both male and female naive mice. During neuropathy, both wild-type (WT) and P2X4KI mice of both sexes develop tactile allodynia accompanied by spinal neuron hyperexcitability. These responses are selectively associated with P2X4, as they are absent in global P2X4KO or myeloid-specific P2X4KO mice. We show that P2X4 is de novo expressed in reactive microglia in neuropathic WT and P2X4KI mice of both sexes and that tactile allodynia is relieved by pharmacological blockade of P2X4 or TrkB. These results show that the upregulation of P2X4 in microglia is crucial for neuropathic pain, regardless of sex.",
author = "Damien Gilabert and Alexia Duveau and Sara Carracedo and Nathalie Linck and Adeline Langla and Rieko Muramatsu and Friedrich Koch-Nolte and Fran{\c c}ois Rassendren and Thomas Grutter and Pascal Fossat and Eric Bou{\'e}-Grabot and Lauriane Ulmann",
note = "{\textcopyright} 2023 The Author(s).",
year = "2023",
month = nov,
day = "17",
doi = "10.1016/j.isci.2023.108110",
language = "English",
volume = "26",
pages = "108110",
journal = "ISCIENCE",
issn = "2589-0042",
publisher = "Elsevier Inc.",
number = "11",

}

RIS

TY - JOUR

T1 - Microglial P2X4 receptors are essential for spinal neurons hyperexcitability and tactile allodynia in male and female neuropathic mice

AU - Gilabert, Damien

AU - Duveau, Alexia

AU - Carracedo, Sara

AU - Linck, Nathalie

AU - Langla, Adeline

AU - Muramatsu, Rieko

AU - Koch-Nolte, Friedrich

AU - Rassendren, François

AU - Grutter, Thomas

AU - Fossat, Pascal

AU - Boué-Grabot, Eric

AU - Ulmann, Lauriane

N1 - © 2023 The Author(s).

PY - 2023/11/17

Y1 - 2023/11/17

N2 - In neuropathic pain, recent evidence has highlighted a sex-dependent role of the P2X4 receptor in spinal microglia in the development of tactile allodynia following nerve injury. Here, using internalization-defective P2X4mCherryIN knockin mice (P2X4KI), we demonstrate that increased cell surface expression of P2X4 induces hypersensitivity to mechanical stimulations and hyperexcitability in spinal cord neurons of both male and female naive mice. During neuropathy, both wild-type (WT) and P2X4KI mice of both sexes develop tactile allodynia accompanied by spinal neuron hyperexcitability. These responses are selectively associated with P2X4, as they are absent in global P2X4KO or myeloid-specific P2X4KO mice. We show that P2X4 is de novo expressed in reactive microglia in neuropathic WT and P2X4KI mice of both sexes and that tactile allodynia is relieved by pharmacological blockade of P2X4 or TrkB. These results show that the upregulation of P2X4 in microglia is crucial for neuropathic pain, regardless of sex.

AB - In neuropathic pain, recent evidence has highlighted a sex-dependent role of the P2X4 receptor in spinal microglia in the development of tactile allodynia following nerve injury. Here, using internalization-defective P2X4mCherryIN knockin mice (P2X4KI), we demonstrate that increased cell surface expression of P2X4 induces hypersensitivity to mechanical stimulations and hyperexcitability in spinal cord neurons of both male and female naive mice. During neuropathy, both wild-type (WT) and P2X4KI mice of both sexes develop tactile allodynia accompanied by spinal neuron hyperexcitability. These responses are selectively associated with P2X4, as they are absent in global P2X4KO or myeloid-specific P2X4KO mice. We show that P2X4 is de novo expressed in reactive microglia in neuropathic WT and P2X4KI mice of both sexes and that tactile allodynia is relieved by pharmacological blockade of P2X4 or TrkB. These results show that the upregulation of P2X4 in microglia is crucial for neuropathic pain, regardless of sex.

U2 - 10.1016/j.isci.2023.108110

DO - 10.1016/j.isci.2023.108110

M3 - SCORING: Journal article

C2 - 37860691

VL - 26

SP - 108110

JO - ISCIENCE

JF - ISCIENCE

SN - 2589-0042

IS - 11

ER -