Retigabine reduces the excitability of unmyelinated peripheral human axons

Expression, Localization, and Pharmacological Role of Kv7 Potassium Channels in Skeletal Muscle Proliferation, Differentiation, and Survival after Myotoxic Insults

“…First, K v 7 channels only contribute to a limited amount of outward current, and therefore their blockade does not significantly influence C 2 C 12 cell membrane potential. The fact that K v 7 channels are not strongly active at the resting membrane potential, but only become so when activated by retigabine, has already been described in peripheral unmyelinated Ctype nerve fibers (Lang et al, 2008) and in central myelinated axons (Rivera-Arconada and Lopez-Garcia, 2006;Vervaeke et al, 2006). Moreover, it should be emphasized that XE-991 was used in the present experiments at 10 M; although this concentration causes an almost complete block of homomeric or heteromeric K v 7.2 or K v 7.3 channels (Wang et al, 1998), K v 7.4 (Søgaard et al, 2001), and, even more so, K v 7.5 (Yeung et al, 2008b) channels display a much lower sensitivity to blockade by XE-991.…”

The acute nociceptive signals induced by bradykinin in rat sensory neurons are mediated by inhibition of M-type K+ channels and activation of Ca2+-activated Cl– channels

“…Accordingly, M channel inhibition depolarizes neurons, making them more excitable, while M current augmentation has the opposite effect (20,(36)(37)(38). Growing evidence suggests that functional M channels are expressed in peripheral sensory fibers and their activity strongly contributes to fiber excitability in vivo (22,(39)(40)(41)(42). Here we show that BK inhibits M current in nociceptors, that M current inhibition is excitatory and causes nociception, and that the nociceptive effect of BK could be attenuated by the pre-application of a specific M channel opener (Figure 8).…”

Involvement of inward rectifier and M-type currents in carbachol-induced epileptiform synchronization

“…These results suggest that although K M does not provide a major contribution to resting excitability in the EC, it participates in sustaining neuronal hyperexcitability during CCh exposure. Interestingly, previous studies have shown that the contribution of K M to resting membrane potential vary among different neuronal populations; in fact while the blockade of K M increased resting excitability in rat visceral sensory neurons (Wladyka and Kunze, 2006) it failed to do so in peripheral unmyelinated C-type nerve fibers (Lang et al, 2008) and in central myelinated axons (Rivera-Arconada and Lopez-Garcia, 2005). Our evidence that the contribution of K M in the control of membrane excitability becomes relevant when the slices are exposed to CCh is consistent with the data reported by Yoshida and Alonso (2007) who showed that K M blockers markedly modify the intrinsic firing properties of EC neurons when they are depolarized.…”