Protein posttranslational modification regulates synaptic protein stability, sorting and trafficking, and is involved in emotional disorders. Yet the molecular mechanisms regulating emotional disorders remain unelucidated. Here we report unknown roles of protein palmitoylation/nitrosylation crosstalk in regulating anxiety-like behaviors in rats. According to the percentages of open arm duration in the elevated plus maze test, the rats were divided into high-, intermediate- and low-anxiety groups. The palmitoylation and nitrosylation levels were detected by acyl-biotin exchange assay, and we found low palmitoylation and high nitrosylation levels in the basolateral amygdala (BLA) of high-anxiety rats. Furthermore, we observed that 2-bromopalmitate (2-BP), a palmitoylation inhibitor, induced anxiety-like behaviors, accompanied with decreased amplitude and frequency of mEPSCs and mIPSCs in the BLA. Additionally, we also found that inhibiting nNOS activity with 7-nitroindazole (7-NI) in the BLA caused anxiolytic effects and reduced the synaptic transmission. Interestingly, diazepam (DZP) rapidly elevated the protein palmitoylation level and attenuated the protein nitrosylation level in the BLA. Specifically, similar to DZP, the voluntary wheel running exerted DZP-like anxiolytic action, and induced high palmitoylation and low nitrosylation levels in the BLA. Lastly, blocking the protein palmitoylation with 2-BP induced an increase in protein nitrosylation level, and attenuating the nNOS activity by 7-NI elevated the protein palmitoylation level. Collectively, these results show a critical role of protein palmitoylation/nitrosylation crosstalk in orchestrating anxiety behavior in rats, and it may serve as a potential target for anxiolytic intervention.

Deficits in astrocyte function contribute to major depressive disorder (MDD) and suicide, but the therapeutic effect of directly reactivating astrocytes for depression remains unclear. Here, specific gains and losses of astrocytic cell functions in the medial prefrontal cortex (mPFC) bidirectionally regulate depression-like symptoms. Remarkably, recombinant human Thrombospondin-1 (rhTSP1), an astrocyte-secreted protein, exerted rapidly antidepressant-like actions through tyrosine hydroxylase (Th)/dopamine (DA)/dopamine D2 receptors (D2Rs) pathways, but not dopamine D1 receptors (D1Rs), which was dependent on SH3 and multiple ankyrin repeat domains 3 (Shank3) in the mPFC. TSP1 in the mPFC might have potential as a target for treating clinical depression.

With the establishment of interdisciplinary platforms in medical engineering, the twenty‐first century has witnessed rapid advancements in brain‒computer interface (BCI) technology, demonstrating significant potential in clinical applications. The fundamental framework of BCIs encompasses signal acquisition, preprocessing, feature extraction, signal translation, and control devices. This article explores the applications of BCIs across various disorders, including post‐stroke motor recovery, consciousness disorders, mental health, and neurological diseases. Through technological innovations, BCI technology has assisted patients in overcoming communication and motor impairments resulting from neurological damage. By bypassing damaged neural pathways and enabling bidirectional interactions with brain signals, BCIs facilitate the gradual rehabilitation of motor functions in post‐stroke patients and show promise in treating psychiatric disorders such as depression. Compared with traditional treatment methods, BCI technology has several unique advantages. Despite challenges in signal processing accuracy, hardware stability, and real‐time data processing technology, technological innovation and interdisciplinary collaboration facilitate greater breakthroughs in the near future for BCIs. In summary, the clinical application of BCI technology presents unprecedented opportunities and challenges in modern healthcare, underscoring the need for continued research and development in this area.

Background: The exact nature of the link between breast cancer and meningiomas is unknown, although observational studies have shown a correlation between the two. Using a two‐sample Mendelian randomization (MR) strategy, we aimed to investigate the effect of breast cancer on meningiomas.Methods: Three sets of genetic instruments were utilized in this study based on publicly available genetic summary data. For breast cancer, we selected 62 strongly associated SNPs; separate datasets were curated for HER2‐positive and HER2‐negative subtypes. MR analyses included outlier testing, MR‐Egger regression, MR‐PRESSO, weighted median, and inverse variance weighted approaches.Results: The inverse variance weighted analysis demonstrated significant evidence for breast cancer's effect on meningioma risk (OR = 1.213, 95% CI = 1.054–1.396, p = 0.007), supported by MR‐Egger (OR = 1.456, 95% CI = 1.066–1.988, p = 0.021) though not by the weighted median method (OR = 1.095, 95% CI = 0.914–1.311, p = 0.326). Inverse variance weighting specifically revealed a significant association between HER2‐positive breast cancer and meningioma incidence (OR = 1.203, 95% CI = 1.048–1.381, p = 0.009). Furthermore, breast cancer risk was associated with an increased incidence of malignant meningiomas (OR = 1.64, 95% CI = 1.12–2.40, p = 0.011).Conclusions: This represents the first MR study investigating the causal relationship between breast cancer and meningiomas. Our findings support the hypothesis that breast cancer may increase meningioma risk.