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bioRxiv · 10.1101/208975

Rem2 regulates distinct homeostatic mechanisms in visual circuit plasticity

Moore, A. R.·Richards, S. E.·Kenny, K.·Royer, L.·Chan, U.·Flavahan, K.·Van Hooser, S. D.·Paradis, S.
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Abstract

Activity-regulated genes sculpt neural circuits in response to sensory experience. These calcium-sensitive genes generally fall into two categories: transcription factors and proteins that function at synapses. Yet little is known about activity-regulated, cytosolic proteins that transduce signals between the neuronal membrane and the nucleus. Using the visual system as a model, we investigated the role of the activity-regulated, non-canonical Ras-like GTPase Rem2 in vivo. We demonstrate that Rem2-/- mice fail to exhibit normal ocular dominance plasticity during the critical period. At the circuit level, cortical layer 2/3 neurons in Rem2-/- mice show deficits in both postsynaptic scaling up of excitatory synapses and misregulation of intrinsic excitability. Further, we reveal that Rem2 plays a novel, cell-autonomous role in regulating neuronal intrinsic excitability. Thus, Rem2 is a critical regulator of neural circuit function and distinct homeostatic plasticity mechanisms in vivo.\n\nHIGHLIGHTSO_LIRem2 is required in excitatory cortical neurons for normal ocular dominance plasticity\nC_LIO_LIRem2 regulates postsynaptic homoeostatic synaptic scaling up\nC_LIO_LIRem2 alters the intrinsic excitability of neurons in a cell-autonomous manner\nC_LI

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Moore, A. R., Richards, S. E., Kenny, K., Royer, L., Chan, U., Flavahan, K., Van Hooser, S. D., Paradis, S.. 2017-10-25. Rem2 regulates distinct homeostatic mechanisms in visual circuit plasticity. https://doi.org/10.1101/208975

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