Neurons store information by changing synaptic input weights. In addition, they can adjust their membrane excitability to alter spike output. Here, we demonstrate a role of such "intrinsic plasticity" in behavioral learning in a mouse model that allows us to detect specific consequences of absent excitability modulation. Mice with a Purkinje-cell-specific knockout (KO) of the calcium-activated K+ channel SK2 (L7-SK2) show intact vestibulo-ocular reflex (VOR) gain adaptation but impaired eyeblink conditioning (EBC), which relies on the ability to establish associations between stimuli, with the eyelid closure itself depending on a transient suppression of spike firing. In these mice, the intrinsic plasticity of Purkinje cells is prevented without affecting long-term depression or potentiation at their parallel fiber (PF) input. In contrast to the typical spike pattern of EBC-supporting zebrin-negative Purkinje cells, L7-SK2 neurons show reduced background spiking but enhanced excitability. Thus, SK2 plasticity and excitability modulation are essential for specific forms of motor learning.

Additional Metadata
Persistent URL dx.doi.org/10.1371/journal.pbio.3000596, hdl.handle.net/1765/124213
Journal PL o S Biology (Online)
Citation
Grasselli, G. (Giorgio), Boele, H.J, Titley, H.K. (Heather K.), Bradford, N. (Nora), van Beers, L. (Lisa), Jay, L. (Lindsey), … Hansel, C.R.W. (2020). SK2 channels in cerebellar Purkinje cells contribute to excitability modulation in motor-learning-specific memory traces. PL o S Biology (Online), 18(1). doi:10.1371/journal.pbio.3000596