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Rem2 stabilizes intrinsic excitability and spontaneous firing in visual circuits.

Anna R Moore | Sarah E Richards | Katelyn Kenny | Leandro Royer | Urann Chan | Kelly Flavahan | Stephen D Van Hooser | Suzanne Paradis
eLife | 2018

Sensory experience plays an important role in shaping neural circuitry by affecting the synaptic connectivity and intrinsic properties of individual neurons. Identifying the molecular players responsible for converting external stimuli into altered neuronal output remains a crucial step in understanding experience-dependent plasticity and circuit function. Here, we investigate the role of the activity-regulated, non-canonical Ras-like GTPase Rem2 in visual circuit plasticity. We demonstrate that Rem2-/- mice fail to exhibit normal ocular dominance plasticity during the critical period. At the cellular level, our data establish a cell-autonomous role for Rem2 in regulating intrinsic excitability of layer 2/3 pyramidal neurons, prior to changes in synaptic function. Consistent with these findings, both in vitro and in vivo recordings reveal increased spontaneous firing rates in the absence of Rem2. Taken together, our data demonstrate that Rem2 is a key molecule that regulates neuronal excitability and circuit function in the context of changing sensory experience.

Pubmed ID: 29809135

Associated grants

  • Agency: NINDS NIH HHS, United States
    Id: Ruth L Kirschstein NIH Training Grant T32NS007292
  • Agency: NINDS NIH HHS, United States
    Id: R01 NS065856
  • Agency: NIMH NIH HHS, United States
    Id: K01 MH101639
  • Agency: NINDS NIH HHS, United States
    Id: R01NS065856
  • Agency: NINDS NIH HHS, United States
    Id: T32 NS007292
  • Agency: NICHD NIH HHS, United States
    Id: P30 HD018655
  • Agency: NIMH NIH HHS, United States
    Id: K01MH101639
  • Agency: NIMH NIH HHS, United States
    Id: T32 MH019929
  • Agency: NEI NIH HHS, United States
    Id: EY022122

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