Using single-cell mass spectrometry technology,Zhu et al.[1] recently revealed that a novel intra-neuronal glutamate (GLU) biosynthetic pathway contributes to sunlight ultraviolet (UV)-induced neurobehavioral effects.In the study,moderate UV exposure was found to increase blood levels of urocanic acid (UCA),which may cross the blood-brain barrier (BBB).Subsequently,UCA promotes GLU biosynthesis and release in various brain regions,including motor cortex and hippocampus.Strikingly,UV exposure improves motor learning and object recognition memory.The inhibitor against urocanase,an enzyme critical for the conversion of UCA to GLU,reverses the UV exposure-related neurological effects.Thus,the activation of UCA-GLU metabolic pathway mediates the process of UV-triggered neurobehavioral changes (Fig.1).
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