期刊
FRONTIERS IN NEURAL CIRCUITS
卷 15, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fncir.2021.658343
关键词
astrocytes; optogenetic activation; G protein-coupled receptor; Ca2+ signaling; memory; OptoA1AR
资金
- KAKENHI grants [25640017, 15K14326, 23115522, 26117520, 16H01888, 18H05150]
- HFSP [RGP0036/2014]
- Novo Nordisk Foundation [NNFOC0058058]
- Danmarks Frie Forskningsfond [0134-00107B]
- Lundbeck Foundation
- RIKEN Brain Science Institute
- Grants-in-Aid for Scientific Research [16H01888, 25640017, 26117520, 18H05150, 15K14326] Funding Source: KAKEN
The study demonstrates that GPCR-triggered Ca2+ elevation in cortical astrocytes has causal impacts on neuronal activity and behavior, including neuronal activity inhibition, sensory evoked response depression, behavioral changes, and memory enhancement.
Astrocytes elicit transient Ca2+ elevations induced by G protein-coupled receptors (GPCRs), yet their role in vivo remains unknown. To address this, transgenic mice with astrocytic expression of the optogenetic Gq-type GPCR, Opto alpha 1AR, were established, in which transient Ca2+ elevations similar to those in wild type mice were induced by brief blue light illumination. Activation of cortical astrocytes resulted in an adenosine A1 receptor-dependent inhibition of neuronal activity. Moreover, sensory stimulation with astrocytic activation induced long-term depression of sensory evoked response. At the behavioral level, repeated astrocytic activation in the anterior cortex gradually affected novel open field exploratory behavior, and remote memory was enhanced in a novel object recognition task. These effects were blocked by A1 receptor antagonism. Together, we demonstrate that GPCR-triggered Ca2+ elevation in cortical astrocytes has causal impacts on neuronal activity and behavior.
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