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

• Published in: Journal of Pharmacological Sciences Vol. 103; no. 1; pp. 93 - 102
• Main Authors: Zheng, Taixing, Kakimura, Jun-ichi, Matsutomi, Tomoya, Nakamoto, Chizumi, Ogata, Nobukuni
• Format: Journal Article
• Language: English
• Published: Japan Elsevier B.V 2007; The Japanese Pharmacological Society; Elsevier
• Subjects: Animals; Capsaicin - pharmacology; Cells, Cultured; Dinoprostone - pharmacology; dorsal root ganglion; Drug Resistance; Ganglia, Spinal - drug effects; Ganglia, Spinal - metabolism; inflammatory hyperalgesia; Mice; NAV1.8 Voltage-Gated Sodium Channel; Nystatin - pharmacology; patch clamp recording; prostaglandin E2; Sodium - metabolism; Sodium Channels - drug effects; Sodium Channels - physiology; Tetrodotoxin - pharmacology; tetrodotoxin-resistant Na+ current; inflammatory hyperalgesia; tetrodotoxin-resistant Na+ current; prostaglandin E2; dorsal root ganglion; patch clamp recording
• ISSN: 1347-8613; 1347-8648
• DOI: 10.1254/jphs.FP0061402

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.