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The Journal of Neuroscience, September 7, 2005, 25(36):8209-8216; doi:10.1523/JNEUROSCI.1951-05.2005

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Development/Plasticity/Repair
Reelin Modulates NMDA Receptor Activity in Cortical Neurons

Ying Chen,¹ Uwe Beffert,¹ Mert Ertunc,³ Tie-Shan Tang,² Ege T. Kavalali,^2,3 Ilya Bezprozvanny,² and Joachim Herz¹

Departments of ¹Molecular Genetics and ²Physiology and ³Center for Basic Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas 75390

Reelin, a large protein that regulates neuronal migration during embryonic development, activates a conserved signaling pathway that requires its receptors, very low-density lipoprotein receptor and apolipoprotein E receptor 2, the cytoplasmic adaptor protein Disabled-1 (Dab1), and Src family kinases (SFK). Reelin also markedly enhances long-term potentiation in the adult hippocampus, suggesting that this developmental signaling pathway can physiologically modulate learning and behavior. Here, we show that Reelin can regulate NMDA-type glutamate receptor activity through a mechanism that requires SFKs and Dab1. Reelin mediates tyrosine phosphorylation of and potentiates calcium influx through NMDA receptors in primary wild-type cortical neurons but not in Dab1 knock-out neurons or in cells in which Reelin binding to its receptors is blocked by a receptor antagonist. Inhibition of SFK abolishes Reelin-induced and glutamate-dependent enhancement of calcium influx. We also show that Reelin-induced augmentation of Ca²⁺ entry through NMDA receptors increases phosphorylation and nuclear translocation of the transcription factor cAMP-response element binding protein. Thus, Reelin may physiologically modulate learning and memory by modulating NMDA receptor functions.

Key words: neurotransmission; brain development; Disabled; Apoer2; Vldlr; LTP

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Received May 16, 2005; revised July 28, 2005; accepted July 31, 2005.

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