ArticleFrontiers in pharmacology2026
Cdk5 modulates orofacial pain through P2X2/3 purinergic receptor-mediated signaling in trigeminal neurons.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Cyclin-dependent kinase 5 (Cdk5) plays a critical role in pain transmission by phosphorylating key nociceptive proteins. One of its recently identified substrates, the P2X2 subunit, is part of the P2X2/3 purinergic receptor (P2X2/3R), which is implicated in nociceptive signaling. However, the specific contribution of Cdk5 to purinergic receptor-mediated pain responses remains unclear. This study aimed to investigate the role of Cdk5 in pain responses elicited by α,β-methylene ATP (α,β-meATP), an agonist of P2X2/3R and P2X3R. Methods: Both pharmacological inhibition and genetic loss-of-function approaches were used to assess the role of Cdk5. Calcium (Ca Results: In TG neuron cultures, α,β-meATP evoked both fast and slow Ca Discussion: These findings indicate that Cdk5 modulates orofacial pain by regulating purinergic receptor-mediated signaling in trigeminal neurons. Specifically, Cdk5 appears to influence the functional properties of P2X2-containing channels, most likely P2X2/3 heteromeric receptors, without affecting their membrane expression. This modulation of receptor kinetics may underlie the observed changes in nociceptive behavior, highlighting Cdk5 and P2X receptors as a potential target for pain modulation.
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