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. 2014 Sep 10;8:280. doi: 10.3389/fncel.2014.00280

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Copyright © 2014 Chuang, Huang and Hsueh.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The model of the signaling pathways elucidating Tbr1 upregulation by neuronal activation. Excitatory synaptic transmission driven by bicuculline treatment triggers the activation of the AMPA glutamate receptor. Na⁺ influx through the AMPA receptor depolarizes the plasma membrane and then activates the NMDA receptor. The activation of CaMKII signaling via NMDAR can induce Tbr1 expression perhaps via other activity-dependent transcription factors (TFs). The elevation of the TBR1 protein levels can further upregulate the Grin2b expression following neuronal activation.