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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Luo, Jia Cimarosti, Helena Henley, Jeremy M. Jaafari, Nadia Gonzàlez-gonzàlez, Immaculada M. Jacobs, Susan C. Kantamneni, Sriharsha |
| Description | Author Affiliation: Kantamneni S ( From the School of Biochemistry, Medical Sciences Building, University of Bristol, Bristol BS8 1TD, United Kingdom.) |
| Abstract | Inhibitory $GABA_{B}$ receptors $(GABA_{B}Rs)$ can down-regulate most excitatory synapses in the CNS by reducing postsynaptic excitability. Functional $GABA_{B}Rs$ are heterodimers of $GABA_{B1}$ and $GABA_{B2}$ subunits and here we show that the trafficking and surface expression of $GABA_{B}Rs$ is differentially regulated by synaptic or pathophysiological activation of NMDA receptors (NMDARs). Activation of synaptic NMDARs using a chemLTP protocol increases $GABA_{B}R$ recycling and surface expression. In contrast, excitotoxic global activation of synaptic and extrasynaptic NMDARs by bath application of NMDA causes the loss of surface $GABA_{B}Rs.$ Intriguingly, exposing neurons to extreme metabolic stress using oxygen/glucose deprivation (OGD) increases $GABA_{B1}$ but decreases $GABA_{B2}$ surface expression. The increase in surface $GABA_{B1}$ involves enhanced recycling and is blocked by the NMDAR antagonist AP5. The decrease in surface $GABA_{B2}$ is also blocked by AP5 and by inhibiting degradation pathways. These results indicate that NMDAR activity is critical in $GABA_{B}R$ trafficking and function and that the individual subunits can be separately controlled to regulate neuronal responsiveness and survival. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 10 |
| Volume Number | 289 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2014-03-07 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Neurons Metabolism Receptors, GABA-B Receptors, N-Methyl-D-Aspartate Synapses Animals Cell Survival Cells, Cultured Protein Transport Signal Transduction Stress, Physiological Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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