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Science & Technology

Bidirectional Synaptic Plasticity Regulated by Endogenous regulator-of-Calcineurin (RCAN1)

By 3rd March 2020No Comments

The following study was conducted by Scientists from Département Neurosciences, Groupe de Recherche sur le Système Nerveux Central, Université de Montréal, Montréal, Canada; Centre de Recherche, Centre Hospitalier Universitaire Sainte-Justine, Montréal, Canada. Study is published in Current Biology Journal as detailed below.

Current Biology (2020);

RCAN1 Regulates Bidirectional Synaptic Plasticity


  • Inhibiting GSK3β-dependent phosphorylation of RCAN1 increases synaptic transmission
  • Inhibiting GSK3β-dependent phosphorylation of RCAN1 blocks LTD induction
  • Inhibiting phosphorylation of RCAN1 at a PKA site blocks LTP induction
  • RCAN1 regulates bidirectional synaptic plasticity through its regulation of calcineurin


Synaptic plasticity, with its two most studied forms, long-term potentiation (LTP) and long-term depression (LTD), is the cellular mechanism underlying learning and memory. Although it has been known for two decades that bidirectional synaptic plasticity necessitates a corresponding bidirectional regulation of calcineurin activity, the underlying molecular mechanism remains elusive. Using organotypic hippocampal slice cultures, we show here that phosphorylation of the endogenous regulator-of-calcineurin (RCAN1) by GSK3β underlies calcineurin activation and is a necessary event for LTD induction, while phosphorylation of RCAN1 at a PKA site blocks calcineurin activity, thereby allowing LTP induction. Our results provide a new mechanism for the regulation of calcineurin in bidirectional synaptic plasticity and establish RCAN1 as a “switch” for bidirectional synaptic plasticity.


Current Biology



Dudilot, A., E. Trillaud-Doppia, et al. “RCAN1 Regulates Bidirectional Synaptic Plasticity.” Current Biology.