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Backgrouds  ATP and P2X receptors play important roles in the modulation of trigeminal neuropathic pain, while the role of G protein-coupled P2Y 2  receptors and the underlying mechanisms are less clear. The threshold and frequency of action potentials, fast inactivating transient K +  channels (I A ) are important regulators of membrane excitability in sensory neurons because of its vital role in the control of the spike onset. In this study, pain behavior tests, QT-RT-PCR, immunohistochemical staining, and patch-clamp recording, were used to investigate the role of P2Y 2  receptors in pain behaviour.    Results  In control rats: 1) UTP, an agonist of P2Y 2 /P2Y 4  receptors, caused a significant decrease in the mean threshold intensities for evoking action potentials and a striking increase in the mean number of spikes evoked by TG neurons. 2) UTP significantly inhibited I A  and the expression of Kv1.4, Kv3.4 and Kv4.2 subunits in TG neurons, which could be reversed by the P2 receptor antagonist suramin and the ERK antagonist U0126. In ION-CCI (chronic constriction injury of infraorbital nerve) rats: 1) mRNA levels of Kv1.4, Kv3.4 and Kv4.2 subunits were significantly decreased, while the protein level of phosphorylated ERK was significantly increased. 2) When blocking P2Y 2  receptors by suramin or injection of P2Y2R antisense oligodeoxynucleotides both led to a time- and dose-dependent reverse of allodynia in ION-CCI rats. 3) Injection of P2Y 2  receptor antisense oligodeoxynucleotides induced a pronounced decrease in phosphorylated ERK expression and a significant increase in Kv1.4, Kv3.4 and Kv4.2 subunit expression in trigeminal ganglia.    Conclusions  Our data suggest that inhibition of P2Y 2  receptors leads to down-regulation of ERK-mediated phosphorylation and increase of the expression of I A –related Kv channels in trigeminal ganglion neurons, which might contribute to the clinical treatment of trigeminal neuropathic pain.

Inhibition of G Protein-Coupled P2Y2 Receptor Induced Analgesia in a Rat Model of Trigeminal Neuropathic Pain

Inhibition of G Protein-Coupled P2Y₂ Receptor Induced Analgesia in a Rat Model of Trigeminal Neuropathic Pain