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Published in: The Journal of Headache and Pain 1/2014

Open Access 01-12-2014 | Research article

Effect of genetic deletion and pharmacological antagonism of P2X7 receptors in a mouse animal model of migraine

Authors: Flóra Gölöncsér, Beáta Sperlágh

Published in: The Journal of Headache and Pain | Issue 1/2014

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Abstract

Background

Purine receptors participate in peripheral and central sensitization and are associated with migraine headache. We investigated the role of P2X7 receptor (P2X7) in a nitroglycerin (NTG)-induced mouse model of migraine.

Methods

Intraperitoneal NTG injection (15 mg/kg) triggered thermal hyperalgesia in the hindpaws of wild-type C57BL/6J mice, followed by the induction of c-fos in upper cervical spinal cord and trigeminal nucleus caudalis. The effect of genetic deletion of P2X7 and the selective P2X7 antagonist Brilliant Blue G (BBG) were examined on hyperalgesia and c-fos induction.

Results

NTG decreased the paw withdrawal threshold in both wild-type and P2X7 knockout mice. Nevertheless, subacute BBG treatment (50 mg/kg/day i.p.) completely prevented the effect of NTG in wild-type, but not in knockout mice. Whereas P2X7 deficiency differentially affected the expression of c-fos, the average number of fos-immuno-reactive neurons in trigeminal nucleus caudalis, but not in upper cervical spinal cord was lower in BBG-treated wild-type mice after NTG treatment.

Conclusions

Our results show that P2X7 receptors might participate in the pathogenesis of migraine, although upregulation of other P2X receptors probably compensate for the loss of its action in knockout mice. The data also suggest the therapeutic potential of P2X7 antagonists for the treatment of migraine.
Appendix
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Metadata
Title
Effect of genetic deletion and pharmacological antagonism of P2X7 receptors in a mouse animal model of migraine
Authors
Flóra Gölöncsér
Beáta Sperlágh
Publication date
01-12-2014
Publisher
Springer Milan
Published in
The Journal of Headache and Pain / Issue 1/2014
Print ISSN: 1129-2369
Electronic ISSN: 1129-2377
DOI
https://doi.org/10.1186/1129-2377-15-24

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