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 E(2) (PGE(2)) in dorsal root ganglion (DRG) neurons. However, no information was available on the properties of the novel type of TTX-R Na(+) channel, Na(V)1.
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