Journal
CELL
Volume 173, Issue 7, Pages 1716-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2018.04.014
Keywords
-
Categories
Funding
- National Key R&D Program of China [2016YFC1300500-2, 2016YFA0201300-2]
- National Natural Science Foundation of China [31471014, 91432103, 91649121, 21775143, 21475121, 81701068]
- Strategic Priority Research Program of the Chinese Academy of Sciences [XDB02010000]
- Fundamental Research Funds for the Central Universities
- Major/Innovative Program of Development Foundation of Hefei Center for Physical Science and Technology [2017FXZY006, 2017FXCX003]
- Recruitment Program of Global Experts
Ask authors/readers for more resources
Sunlight exposure is known to affect mood, learning, and cognition. However, the molecular and cellular mechanisms remain elusive. Here, we show that moderate UV exposure elevated blood urocanic acid (UCA), which then crossed the blood-brain barrier. Single-cell mass spectrometry and isotopic labeling revealed a novel intra-neuronal metabolic pathway converting UCA to glutamate (GLU) after UV exposure. This UV-triggered GLU synthesis promoted its packaging into synaptic vesicles and its release at glutamatergic terminals in the motor cortex and hippocampus. Related behaviors, like rotarod learning and object recognition memory, were enhanced after UV exposure. All UV-induced metabolic, electrophysiological, and behavioral effects could be reproduced by the intravenous injection of UCA and diminished by the application of inhibitor or short hairpin RNA (shRNA) against urocanase, an enzyme critical for the conversion of UCA to GLU. These findings reveal a new GLU biosynthetic pathway, which could contribute to some of the sunlight-induced neurobehavioral changes.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available