Abstract
Homeostatic plasticity occurs through diverse cellular and synaptic mechanisms, and extensive investigations over the preceding decade have established Kv2.1 ion channels as key homeostatic regulatory elements in several central neuronal systems. As in these cellular systems, Kv2.1 channels in spinal motoneurons (MNs) localize within large somatic membrane clusters. However, their role in regulating motoneuron activity is not fully established in vivo. We have previously demonstrated marked Kv2.1 channel redistribution in MNs following in vitro glutamate application and in vivo peripheral nerve injury (Romer et al., 2014, Brain Research, 1547:1–15). Here, we extend these findings through the novel use of a fully intact, in vivo rat preparation to show that Kv2.1 ion channels in lumbar MNs rapidly and reversibly redistribute throughout the somatic membrane following 10 min of electrophysiological sensory and/or motor nerve stimulation. These data establish that Kv2.1 channels are remarkably responsive in vivo to electrically evoked and synaptically driven action potentials in MNs, and strongly implicate motoneuron Kv2.1 channels in the rapid homeostatic response to altered neuronal activity.
Highlights
The intrinsic membrane properties of neurons in the central nervous system are controlled, in part, by the tight regulation of membrane-bound ion channels
We have shown that MN Kv2.1 channels dramatically and significantly decluster following glutamate application in vitro and peripheral nerve injury in vivo (Romer et al 2014)
Dorsal root rhizotomy itself causes declustering of Kv2.1 in MNs, indicating that the extent of Kv2.1 channel declustering observed following sciatic nerve stimulation with dorsal root rhizotomy cannot be solely attributed to the antidromic activity of sciatic motor axons
Summary
The intrinsic membrane properties of neurons in the central nervous system are controlled, in part, by the tight regulation of membrane-bound ion channels. The localization of ion channels within certain membrane compartments and/or signaling ensembles is critical to synaptic integration and shaping of firing properties (Deardorff et al 2013, 2014; Romer et al 2014). In mammalian MNs, Kv2.1 channels, which underlie delayed rectifier potassium currents, form distinct clusters that assemble at a variety of cellular locations, including highly regulated signaling ensembles at C-bouton synaptic sites (Deng and Fyffe 2004; Muennich and Fyffe 2004; Wilson et al 2004; Deardorff et al 2013, 2014; Mandikian et al 2014; Romer et al 2014). These unique ion channels undergo essential activity-dependent changes in anatomic and physiologic parameters
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