Regulation of the spontaneous augmentation of Na(V)1.9 in mouse dorsal root ganglion neurons: effect of PKA and PKC pathways.

Sensory neurons in the dorsal root ganglion express two kinds of tetrodotoxin resistant (TTX-R) isoforms of voltage-gated sodium channels, Na(V)1.8 and Na(V)1.9.

Involvement of voltage-gated sodium channel Na(v)1.8 in the regulation of the release and synthesis of substance P in adult mouse dorsal root ganglion neurons.

This study was conducted to determine whether Na(v)1.8 contributes to the release and/or synthesis of substance P (SP) in adult mice dorsal root ganglion (DRG) neurons. The SP released from cultured DRG neurons of Na(v)1.

Prostaglandin E2 has no effect on two components of tetrodotoxin-resistant Na+ current in mouse dorsal root ganglion.

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.

Multiple types of Na(+) currents mediate action potential electrogenesis in small neurons of mouse dorsal root ganglia.

Small (<25 microm in diameter) neurons of the dorsal root ganglion (DRG) express multiple voltage-gated Na(+) channel subtypes, two of which being resistant to tetrodotoxin (TTX). Each subtype mediates Na(+) current with distinct kinetic property. However, it is not known how each type of Na(+) channel contributes to the generation of action potentials in small DRG neurons.

Electrophysiological characterization of the tetrodotoxin-resistant Na+ channel, Na(v)1.9, in mouse dorsal root ganglion neurons.

Small dorsal root ganglion neurons express preferentially the Na+ channel isoform Na(v)1.9 that mediates a tetrodotoxin-resistant (TTX-R) Na+ current. We investigated properties of the Na+ current mediated by Na(v)1.

Use-dependent removal of the 4-aminopyridine-induced block of the transient K+ current in rat dorsal root ganglia.

Effects of 4-aminopyridine (4-AP) on the transient K(+) current (I(A)) was studied in rat sensory neurons using the whole cell patch-clamp technique. The amplitude of I(A) was reduced by 4-AP. The steady-state inactivation curve for I(A) was shifted in the positive direction by 4-AP, suggesting that the blocking action of 4-AP may be attenuated by membrane depolarization.

Molecular diversity of structure and function of the voltage-gated Na+ channels.

A variety of different isoforms of voltage-sensitive Na+ channels have now been identified. The recent three-dimensional analysis of Na+ channels has unveiled a unique and unexpected structure of the Na+ channel protein. Na+ channels can be classified into two categories on the basis of their amino acid sequence, Nav1 isoforms currently comprising nine highly homologous clones and Nax that possesses structure diverging from Nav1, especially in several critical functional motifs.