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Anxiety, a common and devastating mental disorder, has raised widespread interests. The impacts of air pollution on physical health are well known, whereas few studies have explored the association of atmospheric pollution, especially short-term air pollution exposure, with the risk of anxiety disorders. In addition, there are increasing concerns in emerging evidence supporting a possible etiological link. Therefore, our aim was to evaluate the relationship between short-term exposure to atmospheric pollutants and anxiety outpatient visits in Xi'an, a city of northwestern China and a metropolis with relatively heavy air pollution. We collected the data of both daily outpatient visits and daily air pollution (SO 2 , NO 2 , and PM 10) between January 1, 2010 and January 31, 2016 (2222 days). To clarify the association between short-term ambient atmospheric pollution exposure and anxiety outpatient visits, an over-dispersed Poisson generalized additive model was applied by adjusting the day of the week and weather conditions (including temperature, humidity, sunlight hours, and rainfalls). Positive association between gaseous air pollutants (SO 2 and NO 2) and anxiety daily outpatient visits was observed. Moreover, the largest estimated values of both SO 2 and NO 2 were evidence at lag 03 (4-day moving average lag), with 10 μg/m3 increase corresponded to the increase of outpatient anxiety visits at 4.11% (95% CI: 2.15%, 6.06%) for SO 2 and 3.97% (95% CI: 1.90%, 6.06%) for NO 2. However, there was no differences in susceptibility to air pollutants between different genders as well as different ages. Taken together, short-term exposure to ambient air pollutants, especially gaseous air pollutants (NO 2 and SO 2), can be related to higher risk of anxiety outpatient visits. • Short-term ambient air pollution was associated with outpatient anxiety visits. • Positive association was evidenced for SO 2 and NO 2. • No gender and age difference were found in this association. Short-term ambient air pollution and anxiety. [ABSTRACT FROM AUTHOR]

Transient receptor potential vanillic acid 2 (TRPV2) are well recognized for their contributions to neuronal development, cardiac function, immunity and cancer. However, the precise roles for this thermo TRPchannels in neurological disorder remain unknown. In this study, we employed the CRISPR/Cas9 system to generate genetic mutations of TRPV2. Genetic mutation of TRPV2 resulted in autistic-like phenotypes in mice accompanied with the disordered electrical signals recorded by multi-channels in vivo. To determine possible molecular mechanisms, western blotting was further used to assess the possible involvement of several autism-related proteins. The significantly decreased expression of the R2 subunit of the GABA-B receptor in the hippocampus was observed. Together, our findings suggest that genetic mutation of TRPV2 induces autism-like behavior, results in decreased expression of the R2 subunit of the GABA-B receptor. • Genetic mutation of TRPV2 induces autism-like behavior in mice. • Genetic mutation of TRPV2 results in an abnormal EEG. • Genetic mutation of TRPV2 remarkably decreases expression of the R2 subunit of the GABA-B receptor in the hippocampus. [ABSTRACT FROM AUTHOR]

The brain-gut hormone ghrelin and its receptor GHS-R1a, the growth hormone secretagogue receptor 1a, regulates diverse functions of central nervous system including stress response and mood. Both acute and chronic caloric restrictions (CR) were reported to increase endogenous ghrelin level meanwhile regulate anxiety-related behaviors; however, the causal relationship between CR-induced ghrelin elevation and anxiety are not fully established. Here, we introduced an acute (24 h) and a chronic (10wks) CR procedure to both GHS-R1a KO (Ghsr −/− ) mice and WT (Ghsr +/+ ) littermates, and compared their anxiety-related behaviors. We found that acute CR induced anxiolytic and anti-despairing behaviors in Ghsr +/+ mice but not in Ghsr −/− mice. Ad-libitum refeeding abolished the effect of acute CR on anxiety-related behaviors. In contrast, chronic CR for 10wks facilitated despair-like behavior meanwhile inhibited anxiety-like behavior in Ghsr +/+ mice. GHS-R1a deficiency rescued despair-like behavior while did not affect anxiolytic response induced by chronic CR. In addition, we found elevated interleukin-6 (IL-6) in serum of Ghsr +/+ mice after chronic CR, but not in Ghsr −/− mice. Altogether, our findings indicated that acute CR and chronic CR have different impacts on anxiety-related behaviors, and the former is dependent on ghrelin/GHS-R1a signaling while the latter may not always be. In addition, our findings suggested that GHS-R1a-dependent elevation in serum IL-6 might contribute to increased despair-like behavior in chronic CR state. • Fasting for 24 h induced anxiolytic and anti-despairing behaviors in Ghsr +/+ mice, not in Ghsr −/− mice. • Chronic CR for 10wks facilitated despair-like behavior meanwhile inhibited anxiety-like behavior in Ghsr +/+ mice. • GHS-R1a deficiency rescued despair-like behavior while did not affect anxiolytic response induced by chronic CR. • IL-6 in serum was elevated in Ghsr +/+ mice after chronic CR, but not in Ghsr −/− mice. [ABSTRACT FROM AUTHOR]

Previous studies reported that ginsenoside Rg1 (Rg1) exerts antidepressant-like effect in animal models of depression. However, its effect on post-traumatic stress disorder (PTSD) remains elusive; PTSD is a common and costly psychiatric condition with negative cognitive and affective dysfunctions, such as anxiety and depression. In this study, we evaluated the role of Rg1 in a validated mice model of PTSD induced by single-prolonged stress (SPS). Sertraline, one of the FDA-approved medications for PTSD was used as a positive control. Our results showed that SPS exposure led to increased anxiety-like and despair-like behaviors. SPS exposure also caused enhanced contextual fear memory and overgeneralization of learned fear. Sertraline significantly ameliorated those abnormal behaviors induced by SPS, while Rg1 did not. Meanwhile, we found that sertraline but not Rg1 blocked the suppressive effect of SPS on adult neurogenesis in the hippocampus. Consistently, we found that SPS elevated adrenocorticotropic hormone (ACTH) level in the serum, which was inhibited by sertraline but not Rg1. Our results thus demonstrate that Rg1 at a dose used to treat depression may not be effective to rescue behavioral deficits associated with PTSD. • Exposure to single-prolonged stress (SPS) induced PTSD-like behaviors in mice. • Exposure to SPS led to reduced adult neurogenesis and elevated adrenocorticotropic hormone level in serum. • Sertraline ameliorated abnormal behaviors and neurogenesis dysfunction induced by SPS, while Rg1 did not. [ABSTRACT FROM AUTHOR]