Kv2 conductances are not required for C-bouton mediated enhancement of motoneuron output

Neural motor systems have evolved complex circuits that afford animals a range of behaviours essential for survival. C-bouton synapses arising from cholinergic V0C interneurons amplify motoneuron activity via muscarine type 2 receptors, thus increasing muscle contraction force. Recent work in neonatal mouse motoneurons suggests that delayed rectifier currents carried by post-synaptically clustered KV2.1 channels are crucial to C-bouton amplification. Here we use a motoneuron conditional KV2.1 knockout to show that while KV2.1 modulates maximal firing in neonatal mice, its removal minimally affects either mature motoneuron firing or the enhanced firing rates in response to exogenously applied muscarine. In keeping with this, pharmacological blockade of KV2 currents has minimal electrophysiological effects on mature motoneurons. Furthermore, amplification of electromyography activity during high force tasks was unchanged following KV2.1 deletion. We next show that KV2.2 is also expressed by spinal motoneurons and colocalises with KV2.1 opposite C-boutons. We suggest that the primary function of KV2 proteins - KV2.1 and KV2.2 - is non-conducting in motoneurons, and that KV2.2 can function in the absence of KV2.1, perhaps to ensure the integrity of the synapse.