Journal
JOURNAL OF NEUROCHEMISTRY
Volume 132, Issue 6, Pages 677-686Publisher
WILEY-BLACKWELL
DOI: 10.1111/jnc.13038
Keywords
Ca2+ oscillations; extracellular signal-regulated kinase; mGluR5; phosphorylation; protein kinase A
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Funding
- NIH [DA10044, MH090963]
- Narishige Neuroscience Foundation
- Ishibashi Foundation for the Promotion of Science
- [22791149]
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P41GM103314] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [P50MH090963] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [P01DA010044] Funding Source: NIH RePORTER
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Metabotropic glutamate receptor 5 (mGluR5) regulates excitatory post-synaptic signaling in the central nervous system (CNS) and is implicated in various CNS disorders. Protein kinase A (PKA) signaling is known to play a critical role in neuropsychiatric disorders such as Parkinson's disease, schizophrenia, and addiction. Dopamine signaling is known to modulate the properties of mGluR5 in a cAMP-and PKA-dependent manner, suggesting that mGluR5 may be a direct target for PKA. Our study identifies mGluR5 at Ser870 as a direct substrate for PKA phosphorylation and demonstrates that this phosphorylation plays a critical role in the PKA-mediated modulation of mGluR5 functions such as extracellular signal-regulated kinase phosphorylation and intracellular Ca2+ oscillations. The identification of the molecular mechanism by which PKA signaling modulates mGluR5-mediated cellular responses contributes to the understanding of the interaction between dopaminergic and glutamatergic neuronal signaling.
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