P2X4 signalling contributes to hyperactivity but not pain sensitization comorbidity in a mouse model of attention deficit/hyperactivity disorder
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Otros documentos de la autoría: Bou Sader Nehme, Sarah; Sánchez-Sarasúa, Sandra; adel, ramy; Tuifua, Marie; Ali, Awatef; Essawy, Amina; Abdel Salam, Sherine; Hleihel, Walid; Boué-Grabot, Eric; Landry, Marc
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Título
P2X4 signalling contributes to hyperactivity but not pain sensitization comorbidity in a mouse model of attention deficit/hyperactivity disorderAutoría
Fecha de publicación
2024Editor
Frontiers MediaISSN
1663-9812Cita bibliográfica
Bou Sader Nehme S, Sanchez-Sarasua S, Adel R, Tuifua M, Ali A, Essawy AE, Abdel Salam S, Hleihel W, Boué-Grabot E and Landry M (2024), P2X4 signalling contributes to hyperactivity but not pain sensitization comorbidity in a mouse model of attention deficit/ hyperactivity disorder. Front. Pharmacol. 14:1288994. doi: 10.3389/fphar.2023.1288994Tipo de documento
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Resumen
Introduction: Attention deficit/hyperactivity disorder (ADHD) is a common
neurodevelopmental disorder characterized by hyperactivity, inattention, and
impulsivity that often persist until adulthood. Frequent comorbid ... [+]
Introduction: Attention deficit/hyperactivity disorder (ADHD) is a common
neurodevelopmental disorder characterized by hyperactivity, inattention, and
impulsivity that often persist until adulthood. Frequent comorbid disorders
accompany ADHD and two thirds of children diagnosed with ADHD also suffer
from behavioural disorders and from alteration of sensory processing. We recently
characterized the comorbidity between ADHD-like symptoms and pain sensitisation
in a pharmacological mouse model of ADHD, and we demonstrated the implication
of the anterior cingulate cortex and posterior insula. However, few studies have
explored the causal mechanisms underlying the interactions between ADHD and
pain. The implication of inflammatory mechanisms has been suggested but the
signalling pathways involved have not been explored.
Methods: We investigated the roles of purinergic signalling, at the crossroad of
pain and neuroinflammatory pathways, by using a transgenic mouse line that
carries a total deletion of the P2X4 receptor.
Results: We demonstrated that P2X4 deletion prevents hyperactivity in the mouse
model of ADHD. In contrast, the absence of P2X4 lowered thermal pain thresholds
in sham conditions and did not affect pain sensitization in ADHD-like conditions.
We further analysed microglia reactivity and the expression of inflammatory
markers in wild type and P2X4KO mice. Our results revealed that P2X4
deletion limits microglia reactivity but at the same time exerts proinflammatory
effects in the anterior cingulate cortex and posterior insula.
Conclusion: This dual role of P2X4 could be responsible for the differential effects
noted on ADHD-like symptoms and pain sensitization and calls for further studies
to investigate the therapeutic benefit of targeting the P2X4 receptor in
ADHD patients. [-]
Publicado en
Frontiers in Pharmacology 14:1288994Entidad financiadora
Conseil Régional de Nouvelle Aquitaine | European Union-NextGenerationEU | Margarita Salas | Fédération pour la Recherche sur le Cerveau
Código del proyecto o subvención
AAPR2021A-2020-12051410 | ANR-20-CE14-0016 | MGS/2021/33 | UP2021-021 | BRAIN_2030
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info:eu-repo/semantics/openAccess
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