4.3 Article

Transient Astrocytic Gq Signaling Underlies Remote Memory Enhancement

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

  1. KAKENHI grants [25640017, 15K14326, 23115522, 26117520, 16H01888, 18H05150]
  2. HFSP [RGP0036/2014]
  3. Novo Nordisk Foundation [NNFOC0058058]
  4. Danmarks Frie Forskningsfond [0134-00107B]
  5. Lundbeck Foundation
  6. RIKEN Brain Science Institute
  7. Grants-in-Aid for Scientific Research [16H01888, 25640017, 26117520, 18H05150, 15K14326] Funding Source: KAKEN

向作者/读者索取更多资源

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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