Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 289, Issue 21, Pages 14470-14480Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M114.557132
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Funding
- Japanese Ministry of Education, Culture, Sports, Science, and Technology [21200012, 20399554, 24111507, 26111702, 26117502, 23650159, 18077012]
- Uehara Memorial Foundation
- Sumitomo Foundation
- Brain Science Foundation
- Narishige Neuroscience Research Foundation
- Salt Science Research Foundation [13C2]
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [23650159, 18077012, 26117502, 24111507, 26111702, 21200012] Funding Source: KAKEN
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Astrocytes play active roles in the regulation of synaptic transmission. Neuronal excitation can evoke Ca2+ transients in astrocytes, and these Ca2+ transients can modulate neuronal excitability. Although only a subset of astrocytes appears to communicate with neurons, the types of astrocytes that can regulate neuronal excitability are poorly characterized. We found that similar to 30% of astrocytes in the brain express transient receptor potential vanilloid 4 (TRPV4), indicating that astrocytic subtypes can be classified on the basis of their expression patterns. When TRPV4(+) astrocytes are activated by ligands such as arachidonic acid, the activation propagates to neighboring astrocytes through gap junctions and by ATP release from the TRPV4(+) astrocytes. After activation, both TRPV4(+) and TRPV4(-) astrocytes release glutamate, which acts as an excitatory gliotransmitter to increase synaptic transmission through type 1 metabotropic glutamate receptor (mGluR). Our results indicate that TRPV4(+) astrocytes constitute a novel subtype of the population and are solely responsible for initiating excitatory gliotransmitter release to enhance synaptic transmission. We propose that TRPV4(+) astrocytes form a core of excitatory glial assembly in the brain and function to efficiently increase neuronal excitation in response to endogenous TRPV4 ligands.
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