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The Journal of Neuroscience, December 26, 2007, 27(52):14326-14337; doi:10.1523/JNEUROSCI.4433-07.2007

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Cellular/Molecular
NMDA Receptor Activation Potentiates Inhibitory Transmission through GABA Receptor-Associated Protein-Dependent Exocytosis of GABAA Receptors

Kurt C. Marsden,1 Jennifer B. Beattie,1 Jenna Friedenthal,2 and Reed C. Carroll1

1Dominick P. Purpura Department of Neuroscience, Rose Kennedy Center for Mental Retardation, Albert Einstein College of Medicine of Yeshiva University, Bronx, New York 10461, and 2Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, Connecticut 06520

Correspondence should be addressed to Reed C. Carroll, Dominick P. Purpura Department of Neuroscience, Rose Kennedy Center for Mental Retardation, Albert Einstein College of Medicine of Yeshiva University, 1410 Pelham Parkway, Bronx, NY 10461. Email: rcarroll{at}aecom.yu.edu

The trafficking of postsynaptic AMPA receptors (AMPARs) is a powerful mechanism for regulating the strength of excitatory synapses. It has become clear that the surface levels of inhibitory GABAA receptors (GABAARs) are also subject to regulation and that GABAAR trafficking may contribute to inhibitory plasticity, although the underlying mechanisms are not fully understood. Here, we report that NMDA receptor activation, which has been shown to drive excitatory long-term depression through AMPAR endocytosis, simultaneously increases expression of GABAARs at the dendritic surface of hippocampal neurons. This NMDA stimulus increases miniature IPSC amplitudes and requires the activity of Ca2+ calmodulin-dependent kinase II and the trafficking proteins N-ethylmaleimide-sensitive factor, GABA receptor-associated protein (GABARAP), and glutamate receptor interacting protein (GRIP). These data demonstrate for the first time that endogenous GABARAP and GRIP contribute to the regulated trafficking of GABAARs. In addition, they reveal that the bidirectional trafficking of AMPA and GABAA receptors can be driven by a single glutamatergic stimulus, providing a potent postsynaptic mechanism for modulating neuronal excitability.

Key words: synaptic plasticity; GABAA receptor trafficking; CaMKII; NSF; GABARAP; GRIP

Received April 23, 2007; revised Nov. 2, 2007; accepted Nov. 10, 2007.

Correspondence should be addressed to Reed C. Carroll, Dominick P. Purpura Department of Neuroscience, Rose Kennedy Center for Mental Retardation, Albert Einstein College of Medicine of Yeshiva University, 1410 Pelham Parkway, Bronx, NY 10461. Email: rcarroll{at}aecom.yu.edu






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