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BackgroundRecently, concerns about the combined effects of electromagnetic field (EMF) in daily living and occupational environment are rapidly growing.MethodsIn this study, we investigated the combined effects of 1-week exposure to electromagnetic pulse (EMP) at 650 kV/m for 1,000 pulses and 4.9 GHz radiofrequency (RF) at 50 W/m2 for 1 h/d in male mice. Open field test, tail suspension test and Y-maze were applied to evaluate anxiety, depression-like behaviors and spatial memory ability, respectively.ResultsIt was found that compared with Sham group, combined exposure to EMP and RF induced anxiety-like behavior, increased the level of serum S100B and decreased the level of serum 5-HT. The results of quantitative proteomic and KEGG analysis showed that the differentially expressed proteins in hippocampus were enriched in Glutamatergic and GABAergic synapse after combined exposure group, which were verified by western blot. In addition, an obvious histological alteration and autophagy-associated cell death were observed in amygdala instead of hippocampus after combined exposure to EMP and 4.9 GHz RF.ConclusionCombined exposure to EMP and 4.9 GHz RF could induce emotional behavior alteration, which might be associated with Glutamatergic and GABAergic synapse system of hippocampus and autophagy in amygdala.

Light exposure can profoundly affect neurological functions and behaviors. Here, we show that short-term exposure to moderate (400 lux) white light during Y-maze test promoted spatial memory retrieval and induced only mild anxiety in mice. This beneficial effect involves the activation of a circuit including neurons in the central amygdala (CeA), locus coeruleus (LC), and dentate gyrus (DG). Specifically, moderate light activated corticotropin-releasing hormone (CRH) positive (+) CeA neurons and induced the release of corticotropin-releasing factor (CRF) from their axon terminals ending in the LC. CRF then activated tyrosine hydroxylase-expressing LC neurons, which send projections to DG and release norepinephrine (NE). NE activated β-adrenergic receptors on CaMKIIα-expressing DG neurons, ultimately promoting spatial memory retrieval. Our study thus demonstrated a specific light scheme that can promote spatial memory without excessive stress, and unraveled the underlying CeA-LC-DG circuit and associated neurochemical mechanisms.