SK2 channel modulation contributes to compartment-specific dendritic plasticity in cerebellar Purkinje cells

Gen Ohtsuki, Claire Piochon, John P. Adelman, Christian Hansel

Research output: Contribution to journalArticle

55 Scopus citations

Abstract

Small-conductance Ca 2+-activated K + channels (SK channels) modulate excitability and curtail excitatory postsynaptic potentials (EPSPs) in neuronal dendrites. Here, we demonstrate long-lasting plasticity of intrinsic excitability (IE) in dendrites that results from changes in the gain of this regulatory mechanism. Using dendritic patch-clamp recordings from rat cerebellar Purkinje cells, we find that somatic depolarization or parallel fiber (PF) burst stimulation induce long-term amplification of synaptic responses to climbing fiber (CF) or PF stimulation and enhance the amplitude of passively propagated sodium spikes. Dendritic plasticity is mimicked and occluded by the SK channel blocker apamin and is absent in Purkinje cells from SK2 null mice. Triple-patch recordings from two dendritic sites and the soma and confocal calcium imaging studies show that local stimulation limits dendritic plasticity to the activated compartment of the dendrite. This plasticity mechanism allows Purkinje cells to adjust the SK2-mediated control of dendritic excitability in an activity-dependent manner.

Original languageEnglish (US)
Pages (from-to)108-120
Number of pages13
JournalNeuron
Volume75
Issue number1
DOIs
StatePublished - Jul 12 2012

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'SK2 channel modulation contributes to compartment-specific dendritic plasticity in cerebellar Purkinje cells'. Together they form a unique fingerprint.

  • Cite this