Hui Shen

Retinopathy of prematurity (ROP), the leading cause of childhood blindness, is considered a vascular retinopathy; however, clinical studies have reported p

Eye opening represents a critical milestone in postnatal visual development, triggering experience-dependent plasticity that refines neural circuits across visual pathways. While synaptic maturation in the thalamocortical system has been extensively studied, how eye opening shapes synaptic development in the superior colliculus (SC) – a major subcortical hub mediating rapid orienting and motion detection – remains poorly understood. Here, we combine electrophysiological, biochemical, and ultrastructural approaches to investigate experience-promoted synaptic development in the mouse SC following eye opening. We show that eye opening enhances spontaneous AMPAR-mediated synaptic transmission, increasing both the frequency and amplitude of currents. This functional potentiation is accompanied by elevated expression of GluR1, GluR2, and the postsynaptic density protein 95. Structural analyses further reveal enlargement of postsynaptic densities, increased presynaptic vesicle number, and elevated dendritic spine density without altering spine subtype distribution. Our findings demonstrate that eye opening primes robust functional and structural maturation of SC synapses through AMPAR-mediated mechanisms, highlighting the SC as a key site of experience-dependent plasticity with distinct developmental mechanisms in the subcortical visual pathway.

The neuroinflammation plays a crucial role in the pathogenesis and progression of depression. Microglia serve as the principal source of neuroinflammatory factors and regulate neuroinflammation via M1 and M2 polarization phenotypes. Moreover, NOD like receptor protein 3 (NLRP3) inflammasome pathway is considered to be important in regulating pro-inflammatory cytokine release in the hippocampus. Zinc supplementation has been shown to effectively alleviate depressive symptoms in patients. In this study, we utilized a lipopolysaccharide (LPS)-induced mouse model of depression and LPS-activated BV-2 cells to examine the impact of zinc supplementation. The findings indicated that zinc supplementation could: (1) ameliorate the depressive-like behaviors of the mouse model with inhibition of inflammatory cytokines and zinc homeostasis recovery. (2) induce the polarization of microglia towards the M2 phenotype in vivo and in vitro. (3) suppress the activation of the NLRP3 inflammasome pathway by impeding the expression of P2X purinergic receptor 7 (P2 × 7) induced by LPS, thereby regulating microglial polarization. This may represent a crucial pathway via which zinc inhibits the M1 polarization of microglia, promotes polarization towards the M2 phenotype, thus improving neuroinflammation and exerting an antidepressant effect.

Acute sleep deprivation (SD) rapidly alleviates depression, addressing a critical gap in mood disorder treatment. Rapid eye movement SD (REM SD) modulates the excitability of vasoactive intestinal peptide (VIP) neurons, influencing the synaptic plasticity of pyramidal neurons. However, the precise mechanism remains undefined. To investigate this, we used a modified multiple platform method (MMPM) to induce 12 hours of REM SD, specifically targeting VIP neurons in the medial prefrontal cortex (mPFC). Our results show that REM SD mitigated depression by suppressing VIP neurons activity, which directly increased the excitability of pyramidal neurons and, consequently, promoted synaptic plasticity recovery. In addition, the knockdown of VPAC2 on mPFC pyramidal neurons revealed that VPAC2-mediated AC/cAMP/PKA signaling pathway in these neurons is essential for REM SD to mitigate depression-like behavior. These findings suggest that VIP neurons directly regulate pyramidal neurons and are crucial in alleviating depression by REM SD.

Background: Malnutrition and tuberculosis form a mutually reinforcing vicious cycle. While nutritional interventions are crucial for TB management, the knowledge structure and research frontiers remain insufficiently characterised.Objective: To systematically analyse the structure, trajectory and frontiers of research in the nutrition‐tuberculosis field using bibliometric methods.Methods: Relevant literature published since 2007 was retrieved from the Web of Science Core Collection database. CiteSpace was employed to perform multidimensional analyses, including co‐occurrence, cluster timeline visualisation and burst detection for keywords, citations and authors, thereby constructing knowledge maps and identifying key nodes through network centrality metrics.Results: A total of 4502 bibliographic records were analysed. Key findings include: (1) Vitamin D occupies a central position (frequency 326, centrality 70), bridging basic immune mechanisms and clinical applications; (2) research paradigms evolved from molecular mechanism exploration (2007–2012), through clinical translation validation (2011–2019), to systems biology integration (2019–2025); (3) gut microbiota (burst strength 11.73) and (fatty) acids emerged as frontiers; (4) diabetes–tuberculosis comorbidity revealed the complexity of metabolic‐immune interaction networks and (5) high citation frequency of WHO reports indicates a pressing need for translating research into policy.Conclusions: Nutrition–tuberculosis research is shifting from single‐nutrient studies towards integrated ‘nutrition–microbiome–metabolism–immunity’ networks. Vitamin D remains central, but future priorities should focus on precision interventions, multi‐omics integration and translation from mechanism to practice, especially for high‐risk groups.

Status epilepticus (SE) is an acute medical emergency with unclear cellular and circuit mechanisms, and it is imperative to develop anti-SE strategies. Here, we observe distinct astrocytic Ca²⁺ activity patterns during SE: generalized seizures (GS) show synchronized activity between CA3 and contralateral S1, while focal seizures (FS) exhibit desynchronization. Additionally, micrometer-scale wireless electrical stimulation (WES) targeting the medial septum and ventral diagonal band of Broca (MS/vDB) effectively terminates SE and suppresses abnormal astrocytic Ca²⁺ activity, comparable to conventional deep brain stimulation (DBS). The effect is linked to MS/vDB GABAergic neuron activation, which suppresses calcium dynamics within the CA3 astrocyte-pyramidal neuron microcircuit. Meanwhile, WES of the MS/vDB effectively suppresses chronic spontaneous seizures induced by pilocarpine within 10 days. This study shows the divergent patterns of astrocytic activity during SE. It also demonstrates that WES of MS/vDB can effectively suppress SE, establishing an advanced therapeutic strategy.