STIM1 regulates somatic Ca2+ signals and intrinsic firing properties of cerebellar purkinje neurons

Changhyeon Ryu, Dong Cheol Jang, Dayoon Jung, Yong Gyu Kim, Hyun Geun Shim, Hyun Hee Ryu, Yong Seok Lee, David J. Linden, Paul F. Worley, Sang Jeong Kim

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


Control of Ca2+ flux between the cytosol and intracellular Ca2+ stores is essential for maintaining normal cellular function. It has been well established in both neuronal and non-neuronal cells that stromal interaction molecule 1 (STIM1) initiates and regulates refilling Ca2 into the ER. Here, we describe a novel, additional role for STIM1, the regulation of free cytosolic Ca2+, and the consequent control of spike firing in neurons. Among central neurons, cerebellar Purkinje neurons express the highest level of STIM1, and they fire continuously in the absence of stimulation, making somatic Ca2+ homeostasis of particular importance. By using Purkinje neuron-specific STIM1 knock-out (STIM1PKO) male mice, we found that the deletion of STIM1 delayed clearance of cytosolic Ca2+ in the soma during ongoing neuronal firing. Deletion of STIM1 also reduced the Purkinje neuronal excitability and impaired intrinsic plasticity without affecting long-term synaptic plasticity. In vestibulo-ocular reflex learning, STIM1PKO male mice showed severe deficits in memory consolidation, whereas they were normal in memory acquisition. Our results suggest that STIM1 is critically involved in the regulation of the neuronal excitability and the intrinsic plasticity of the Purkinje neurons as well as cerebellar memory consolidation.

Original languageEnglish (US)
Pages (from-to)8876-8894
Number of pages19
JournalJournal of Neuroscience
Issue number37
StatePublished - 2017


  • Cerebellum
  • Intrinsic excitability
  • Intrinsic plasticity
  • Memory consolidation
  • Purkinje neuron
  • STIM1

ASJC Scopus subject areas

  • General Neuroscience


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