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J Neurophysiol (January 17, 2007). doi:10.1152/jn.00869.2006
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Submitted on August 16, 2006
Accepted on January 11, 2007

Reelin signaling facilitates maturation of CA1 glutamatergic synapses

Shenfeng Qiu1 and Edwin J Weeber2*

1 Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, Tennessee, United States
2 Dept. of Molecular Physiology and Biophysics, Vanderbilt University, 702 Light Hall, United States; Dept. of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, United States

* To whom correspondence should be addressed. E-mail: edwin.j.weeber{at}vanderbilt.edu.

Reelin signaling through the low density lipoprotein receptor family members, apoliproprotein E receptor 2 (apoER2) and very low density lipoprotein receptor (VLDLR), plays a pivotal role in dictating neuronal lamination during embryonic brain development. Recent evidence suggests that this signaling system also plays a role in the postnatal brain to modulate synaptic transmission, plasticity and cognitive behavior, mostly likely due to a functional coupling with NMDA receptors. In this study, we investigated the effects of reelin on the maturation of CA1 glutamatergic function using electrophysiological and biochemical approaches. In cultured hippocampal slices, reelin treatment increased the amplitude of AMPAR-mediated miniature EPSCs and the evoked AMPA/NMDA receptor current ratios. In addition, reelin treatment also reduced the number of silent synapses, facilitated a developmental switch from NR2B to NR2A of NMDARs, and increased surface expression of AMPARs in CA1 tissue. In cultured hippocampal neurons from reeler embryos, reduced numbers of AMPAR subunit GluR1 and NMDAR subunit NR1 clustering were observed compared with those obtained from wild type embryos. Supplementing reelin in the reeler culture obliterated these genotypic differences. These results demonstrate that reelin- and lipoprotein receptor-mediated signaling may operate during developmental maturation of hippocampal glutamatergic function and thus represent a potential important mechanism for controlling synaptic strength and plasticity in the postnatal hippocampus.




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