Does prostaglandin upregulate the tetrodotoxin-resistant Na~+ current in DRG neurons?

摘要

One possible mechanism underlying the inflammation-induced sensiti-zation of primary afferent neurons 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 E_2 (PGE_2) in dorsal root ganglion (DRG) neurons. However, no information was available on the property of the novel type of TTX-R Na~+ channel, Na_v1.9, at the time when these reports were published. Hence, the contribution of Na_v1.9 to the PGE_2-induced upregulation of TTX-R Na~+ current remains to be elucidated. To further examine the modulation of TTX-R Na~+ current by PGE_2, two components of TTX-R Na~+ current have been recorded in isolation from small (<25nm 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 PGE_2 (1 and10