K_v2.1 and silent K_v subunits underlie the delayed rectifier K⁺ current in cultured small mouse DRG neurons

Abstract

Silent voltage-gated K+ (Kv) subunits interact with Kv2 subunits and primarily modulate the voltage dependence of inactivation of these heterotetrameric channels. Both Kv2 and silent Kv subunits are expressed in the mammalian nervous system, but little is known about their expression and function in sensory neurons. This study reports the presence of Kv2.1, Kv2.2, and silent subunit Kv6.1, Kv8.1, Kv9.1, Kv9.2, and Kv9.3 mRNA in mouse dorsal root ganglia (DRG). Immunocytochemistry confirmed the protein expression of Kv2.x and Kv9.x subunits in cultured small DRG neurons. To investigate if Kv2 and silent Kv subunits are underlying the delayed rectifier K+ current ( IK) in these neurons, Kv2-mediated currents were isolated by the extracellular application of rStromatoxin-1 (ScTx) or by the intracellular application of Kv2 antibodies. Both ScTx- and anti-Kv2.1-sensitive currents displayed two components in their voltage dependence of inactivation. Together, both components accounted for approximately two-thirds of IK. A comparison with results obtained in heterologous expression systems suggests that one component reflects homotetrameric Kv2.1 channels, whereas the other component represents heterotetrameric Kv2.1/silent Kv channels. These observations support a physiological role for silent Kv subunits in small DRG neurons.

Sialic Acids Attached to O-Glycans Modulate Voltage-gated Potassium Channel Gating

“…In- stead, the steady-state inactivation curves shown in Fig. 4B are similar to that reported by others in recent studies using comparable pulse protocols to measure K v 2.1 inactivation in other mammalian cells (29,(43)(44)(45)(46)(47).…”

“…To discern the effects of glycosylation on K v 2.1 steady-state slow inactivation, cells were pre-pulsed from Ϫ110 mV to ϩ40 mV (10 mV increments) for 5 s, stepped to ϩ30 mV for 500 ms, and returned to the holding potential (Ϫ120 mV) for 15 s, similar to that described previously (28,29).…”

Effect of lysophosphatidic acid on the immune inflammatory response and the connexin 43 protein in myocardial infarction

“…It was deduced that LPA had a dose-dependent effect on the K v current. The electrophysiological characteristics (current amplitude and activation, and inactivation voltage range) of K v in the present study were concordant with those of previous reports (14,15). (Fig.…”

Non-conducting function of the Kv2.1 channel enables it to recruit vesicles for release in neuroendocrine and nerve cells

“…The importance of somatic release in neurons has been described for several types of neuron (Chen et al, 1995;Dan et al, 1994;Sun and Poo, 1987), including dorsal-root-ganglions (DRGs) (Bao et al, 2003;Huang and Neher, 1996;Zhang and Zhou, 2002). Specifically, regulation of release of pain-related peptides stored in LDCVs in cell bodies of small DRGs (Zhang et al, 1995) may contribute to primary sensation and pain (Zheng et al, 2009 (Bocksteins et al, 2009) and which undergo robust Ca 2+ -regulated exocytosis (Huang and Neher, 1996). We demonstrate that Kv2.1 channels in small DRGs physically interact with syntaxin and induce facilitation of release.…”