Prostaglandin E₂ Has No Effect on Two Components of Tetrodotoxin-Resistant Na⁺ Current in Mouse Dorsal Root Ganglion

抄録

One possible mechanism underlying inflammation-induced sensitization of the primary afferent neuron is the upregulation of tetrodotoxin-resistant (TTX-R) Na⁺ current by inflammatory mediators such as prostaglandins. This notion is based on reports that showed an augmentation of TTX-R Na⁺ current following an application of prostaglandin E₂ (PGE₂) in dorsal root ganglion (DRG) neurons. However, no information was available on the properties of the novel type of TTX-R Na⁺ channel, Na_V1.9, at times when these reports were published. Hence, the contribution of Na_V1.9 to the PGE₂-induced upregulation of TTX-R Na⁺ current remains to be elucidated. To further examine the modulation of TTX-R Na⁺ current by PGE₂, we recorded two components of TTX-R Na⁺ current in isolation from small (<25 μm in diameter) DRG neurons using wild-type and Na_V1.8 knock-out mice. Unexpectedly, neither the component mediated by Na_V1.8 nor the persistent component mediated by Na_V1.9 was affected by PGE₂ (1 and 10 μM). Our results raise a question regarding the well-known modulatory role of PGE₂ on TTX-R Na⁺ current in inflammatory hyperalgesia.