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The Journal of Neuroscience, September 15, 2002, 22(18):8042-8051

The AMPA Receptor Subunit GluR1 Regulates Dendritic Architecture of Motor Neurons

Fiona M. Inglis¹, Richard Crockett¹, Sailaja Korada¹, Wickliffe C. Abraham³, Michael Hollmann⁴, and Robert G. Kalb^{1, 2}

Departments of ¹ Neurology and ² Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06520-8018, ³ Department of Psychology, University of Otago, Dunedin, New Zealand, and ⁴ Department of Biochemistry I-Receptor Biochemistry, Ruhr University Bochum, D-44780, Bochum, Germany

The morphology of the mature motor neuron dendritic arbor is determined by activity-dependent processes occurring during a critical period in early postnatal life. The abundance of the AMPA receptor subunit GluR1 in motor neurons is very high during this period and subsequently falls to a negligible level. To test the role of GluR1 in dendrite morphogenesis, we reintroduced GluR1 into rat motor neurons at the end of the critical period and quantitatively studied the effects on dendrite architecture. Two versions of GluR1 were studied that differed by the amino acid in the "Q/R" editing site. The amino acid occupying this site determines single-channel conductance, ionic permeability, and other essential electrophysiologic properties of the resulting receptor channels. We found large-scale remodeling of dendritic architectures in a manner depending on the amino acid occupying the Q/R editing site. Alterations in the distribution of dendritic arbor were not prevented by blocking NMDA receptors. These observations suggest that the expression of GluR1 in motor neurons modulates a component of the molecular substrate of activity-dependent dendrite morphogenesis. The control of these events relies on subunit-specific properties of AMPA receptors.

Key words: activity-dependent development; motor neuron; dendrite; glutamate receptor; AMPA receptor; NMDA receptor; RNA editing; spinal cord

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Copyright © 2002 Society for Neuroscience  0270-6474/02/22188042-10$05.00/0

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