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 K_V2.1 channels is crucial to C-bouton amplification. By focusing on more mature motoneurons, we show that conditional knockout of K_V2.1 channels minimally affects either excitability or response to exogenously applied muscarine. Similarly, unlike in neonatal motoneurons or cortical pyramidal neurons, pharmacological blockade of K_V2 currents has minimal effect on mature motoneuron firing in vitro. Furthermore, in vivo amplification of electromyography activity and high-force task performance was unchanged following K_V2.1 knockout. Finally, we show that K_V2.2 is also expressed by spinal motoneurons, colocalizing with K_V2.1 opposite C-boutons. We suggest that the primary function of K_V2 proteins in motoneurons is non-conducting and that K_V2.2 can function in this role in the absence of K_V2.1.