| Summary: | 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, NaV1.9, at times when these reports were published. Hence, the contribution of NaV1.9 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 NaV1.8 knock-out mice. Unexpectedly, neither the component mediated by NaV1.8 nor the persistent component mediated by NaV1.9 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. Keywords:: prostaglandin E2, tetrodotoxin-resistant Na+ current, dorsal root ganglion, inflammatory hyperalgesia, patch clamp recording
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