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

Abstract Neural motor systems have evolved complex circuits that afford animals a range of behaviours essential for survival. C-bouton synapses arising from cholinergic V0 C 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 K V 2.1 channels are crucial to C-bouton amplification. Here we use a motoneuron conditional K V 2.1 knockout to show that while K V 2.1 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 K V 2 currents has minimal electrophysiological effects on mature motoneurons. Furthermore, amplification of electromyography activity during high force tasks was unchanged following K V 2.1 deletion. We next show that K V 2.2 is also expressed by spinal motoneurons and colocalises with K V 2.1 opposite C-boutons. We suggest that the primary function of K V 2 proteins – K V 2.1 and K V 2.2 – is non-conducting in motoneurons, and that K V 2.2 can function in the absence of K V 2.1, perhaps to ensure the integrity of the synapse.