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The Journal of Neuroscience, October 8, 2008, 28(41):10220-10233; doi:10.1523/JNEUROSCI.3434-08.2008

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Cellular/Molecular
GluR1 Controls Dendrite Growth through Its Binding Partner, SAP97

Weiguo Zhou,¹ Lei Zhang,¹ Xiong Guoxiang,¹ Jelena Mojsilovic-Petrovic,¹ Kogo Takamaya,² Rita Sattler,^2,3 Richard Huganir,² and Robert Kalb¹

¹Department of Pediatrics, Division of Neurology, Joseph Stokes Jr. Research Institute, Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, ²Department of Neuroscience and Howard Hughes Medical Institute, Johns Hopkins University, Baltimore, Maryland 21205, and ³Department of Neurology, Johns Hopkins University, Baltimore, Maryland 21287

Correspondence should be addressed to Dr. Robert Kalb, Joseph Stokes Jr. Research Institute, Children's Hospital of Philadelphia, 3615 Civic Center Boulevard, Philadelphia, PA 19104. Email: kalb{at}email.chop.edu

Activity-dependent dendrite elaboration influences the pattern of interneuronal connectivity and network function. In the present study, we examined the mechanism by which the GluR1 subunit of AMPA receptors controls dendrite morphogenesis. GluR1 binds to SAP97, a scaffolding protein that is a component of the postsynaptic density, via its C-terminal 7 aa. We find that elimination of this interaction in vitro or in vivo (by deleting the C-terminal 7 aa of GluR1, GluR17) does not influence trafficking, processing, or cell surface GluR1 expression but does prevent translocation of SAP97 from the cytosol to membranes. GluR1 and SAP97 together at the plasma membrane promotes dendrite branching in an activity-dependent manner, although this does not require physical association. Our findings suggest that the C-terminal 7 aa of GluR1 are essential for bringing SAP97 to the plasma membrane, where it acts to translate the activity of AMPA receptors into dendrite growth.

Key words: motor neurons; spinal cord; synaptic activity; postsynaptic density; trafficking; scaffold protein

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Received July 22, 2008; accepted Aug. 11, 2008.

Correspondence should be addressed to Dr. Robert Kalb, Joseph Stokes Jr. Research Institute, Children's Hospital of Philadelphia, 3615 Civic Center Boulevard, Philadelphia, PA 19104. Email: kalb{at}email.chop.edu

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