Figure 1. Making antisense of Kcna2 in pain. Pain sensation involves transmission of signals by sensory nerves through the spinal cord to motor nerves, which control the physiological motor response.

(I) In normal neurons, potassium channel Kv1.2 (Kcna2) mRNA [a] is produced in sensory nerve cell bodies that lie in the dorsal root ganglia (DRG), leading to expression of Kcna2 voltage-gated potassium channels [b]. The resulting potassium channel conductance counterbalances the sodium influx, stabilizing the neuronal membrane and enabling normal neuronal firing [c].

(II) In injured nerves, antisense Kcna2 lncRNA is upregulated [a] and silences normal expression of Kcna2 voltage-gated potassium channels [b]. The reduced potassium conductance alters the balance of ion fluxes, which decreases the threshold for action potential firing compared with that in uninjured nerves and creates hyperexcitable neurons [c].