| First Author | Smith CC | Year | 2024 |
| Journal | iScience | Volume | 27 |
| Issue | 8 | Pages | 110444 |
| PubMed ID | 39148717 | Mgi Jnum | J:353818 |
| Mgi Id | MGI:7714154 | Doi | 10.1016/j.isci.2024.110444 |
| Citation | Smith CC, et al. (2024) Kv2 channels do not function as canonical delayed rectifiers in spinal motoneurons. iScience 27(8):110444 |
| abstractText | 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(V)2.1 channels is crucial to C-bouton amplification. By focusing on more mature motoneurons, we show that conditional knockout of K(V)2.1 channels minimally affects either excitability or response to exogenously applied muscarine. Similarly, unlike in neonatal motoneurons or cortical pyramidal neurons, pharmacological blockade of K(V)2 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(V)2.1 knockout. Finally, we show that K(V)2.2 is also expressed by spinal motoneurons, colocalizing with K(V)2.1 opposite C-boutons. We suggest that the primary function of K(V)2 proteins in motoneurons is non-conducting and that K(V)2.2 can function in this role in the absence of K(V)2.1. |
