M-current inhibition rapidly induces a unique CK2-dependent plasticity of the axon initial segment.

ABSTRACT: Alterations in synaptic input, persisting for hours to days, elicit homeostatic plastic changes in the axon initial segment (AIS), which is pivotal for spike generation. Here, in hippocampal pyramidal neurons of both primary cultures and slices, we triggered a unique form of AIS plasticity by selectively targeting M-type K⁺ channels, which predominantly localize to the AIS and are essential for tuning neuronal excitability. While acute M-current inhibition via cholinergic activation or direct channel block made neurons more excitable, minutes to hours of sustained M-current depression resulted in a gradual reduction in intrinsic excitability. Dual soma-axon patch-clamp recordings combined with axonal Na⁺ imaging and immunocytochemistry revealed that these compensatory

SUBMITTER: Lezmy J 

PROVIDER: S-EPMC5703290 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature