Journal
JOURNAL OF NEUROSCIENCE
Volume 27, Issue 52, Pages 14326-14337Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4433-07.2007
Keywords
synaptic plasticity; GABA(A) receptor trafficking; CaMKII; NSF; GABARAP; GRIP
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Funding
- NINDS NIH HHS [NS 049661] Funding Source: Medline
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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 GABA(A) receptors (GABA(A)Rs) are also subject to regulation and that GABA(A)R 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 GABA(A) receptors can be driven by a single glutamatergic stimulus, providing a potent postsynaptic mechanism for modulating neuronal excitability.
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