NS5806 reduces carrageenan-evoked inflammation by suppressing extracellular signal-regulated kinase activation in primary sensory neurons and immune cells.

Background: The compound NS5806 attenuates neuropathic pain via inhibiting extracellular signal-regulated kinase (ERK) activation in neuronal somata located at the dorsal root ganglion (DRG) and superficial spinal dorsal horn. NS5806 also reduces the expansion of DRG macrophages and spinal microglia several days after peripheral nerve injury, implying an anti-inflammatory effect.

Methods: To test whether NS5806 inhibits inflammation, as a model we intraplantarly injected carrageenan into a hind paw of the rat.

NS5806 inhibits ERK activation to attenuate pain induced by peripheral nerve injury.

Neuropathic pain is a serious health problem, but optimal drug treatments remain lacking. It has been known that the compound NS5806 is a Kv4.3 activator, which increases Kv4.

K channel Kv4.1 is expressed in the nociceptors/secondary nociceptive neurons and participates in pain regulation.

Background: Kv4 channels are key components controlling neuronal excitability at membrane potentials below action potential thresholds. It remains elusive whether Kv4.1 participates in pain regulation.

K Channel Modulatory Subunits KChIP and DPP Participate in Kv4-Mediated Mechanical Pain Control.

The K channel pore-forming subunit Kv4.3 is expressed in a subset of nonpeptidergic nociceptors within the dorsal root ganglion (DRG), and knockdown of Kv4.3 selectively induces mechanical hypersensitivity, a major symptom of neuropathic pain.

K Channel Kv3.4 Is Essential for Axon Growth by Limiting the Influx of Ca into Growth Cones.

Membrane excitability in the axonal growth cones of embryonic neurons influences axon growth. Voltage-gated K (Kv) channels are key factors in controlling membrane excitability, but whether they regulate axon growth remains unclear. Here, we report that Kv3.