Kv2 channels do not function as canonical delayed rectifiers in spinal motoneurons.

The increased muscular force output required for some behaviors is achieved via amplification of motoneuron output via cholinergic C-bouton synapses. Work in neonatal mouse motoneurons suggested that modulation of currents mediated by post-synaptically clustered K2.1 channels is crucial to C-bouton amplification. By focusing on more mature motoneurons, we show that conditional knockout of K2.1 channels minimally affects either excitability or response to exogenously applied muscarine. Similarly, unlike in neonatal motoneurons or cortical pyramidal neurons, pharmacological blockade of K2 currents has minimal effect on mature motoneuron firing . Furthermore, amplification of electromyography activity and high-force task performance was unchanged following K2.1 knockout. Finally, we show that K2.2 is also expressed by spinal motoneurons, colocalizing with K2.1 opposite C-boutons. We suggest that the primary function of K2 proteins in motoneurons is non-conducting and that K2.2 can function in this role in the absence of K2.1.