Thursday, July 25, 2013
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.
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].
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].