Transcriptome analysis reveals the immune responses of leopard coral grouper to nervous necrosis virus infectionWang, Yu, Song
et alFish Shellfish Immunol (2025)
Abstract: The leopard coral grouper (Plectropomus leopardus) is a key marine aquaculture species that is vulnerable to nervous necrosis virus infection during its larval stage. This infection often causes viral nervous necrosis disease, resulting in significant losses in aquaculture. The brain tissue serves as a target organ for viral invasion in fish, with vacuolization being the most prominent characteristic observed in susceptible individuals. In this study, a transcriptome analysis was conducted using brain tissues from naturally resistant and susceptible P. leopardus to investigate the defensive mechanisms against nervous necrosis virus infection. Histological observations revealed irregular vacuolization in the brains of fish infected with the nervous necrosis virus. Based on the differentially expressed genes, our study revealed a significant upregulation pathway of neuroactive ligand-receptor interaction, glutamatergic synapse, and GABAergic synapse in the resistant group, while COVID-19 infection pathway and NF-kappa B signaling pathway were primarily downregulated in the susceptible group. These findings suggest that neuroprotective and repair mechanisms may enhance resistance to viral infection while suppressing the immune response, thereby preventing hyperactive damage caused by inflammation. The expression profiles of key differentially expressed genes were validated using qRT-PCR. These genes include those related to the nervous system (grin2b, id4, mpz, sema6bb, dab1a, and nmda2d), cytokine interaction (ccr7), and antigen processing and presentation (hsp90aa1). Fluorescence in situ hybridization (FISH) demonstrated virus co-localization at both the tissue and cellular levels. These findings provide insights into the immune mechanism of leopard coral grouper, aiding in the prevention and treatment of nervous necrosis virus infection.Copyright © 2025. Published by Elsevier Ltd.
Gene mutations linked to drug-resistant epilepsy in astrocytomaPhabphal, Kaewborisutsakul, Leetanaporn
et alFront Neurol (2025) 16, 1523468
Abstract: Epilepsy is common in gliomas, particularly astrocytomas, even in patients who have undergone total tumor resection. Resistance to antiseizure drugs presents a significant challenge in managing epilepsy. Seizure outcomes after brain surgery for drug-resistant epilepsy (DRE) are heterogeneous and difficult to predict using models that evaluate current clinical, imaging, and electrophysiological variables. This study aimed to investigate possible correlations between genetic mutations and antiseizure resistance using whole-exome sequencing.Tumor samples from a medical biobank were subjected to whole-exome sequencing, and the contribution of 64 genes from a previous report was analyzed.Fifteen patients had DRE. Compared to the patients who showed drug responsiveness, patients in the DRE group exhibited mutations in glutamate receptor genes (GRIA1, GRIK5, GRIN2B, or GRIN2C), ATRX, and the glutamate-S-transferase gene. No significant differences were found between the groups in terms of mutations in BRAF, Olig2, Ki-67, IDH, PIK3CA, p53, GRM, or BCL2A.These findings suggest that somatic gene mutations are closely linked to DRE. Identifying the molecular basis of antiseizure drug resistance is crucial for improving the management of DRE.Copyright © 2025 Phabphal, Kaewborisutsakul, Leetanaporn, Choochuen, Tunthanathip, Navakanitworakul and Sangkhathat.
The effects of risperidone and voluntary exercise intervention on synaptic plasticity gene expressions in the hippocampus and prefrontal cortex of juvenile female ratsYi, Sylvester, Lian
et alPhysiol Behav (2025) 294, 114879
Abstract: Psychiatric disorders and antipsychotics are associated with impaired neuroplasticity, while physical exercise has been reported to enhance neuroplasticity and improve cognitive and affective processes. Therefore, this study hypothesizes that voluntary exercise can enhance synaptic plasticity in juvenile rats disrupted by risperidone, a commonly prescribed antipsychotic for pediatric patients.Thirty-two juvenile female rats were randomly assigned to Vehicle+Sedentary, Risperidone (0.9mg/kg; b.i.d)+Sedentary, Vehicle+Exercise (three hours daily access to running wheels), and Risperidone+Exercise groups for four week treatment. Brains were collected for further analysis.In the hippocampus, the mRNA expressions of Bdnf, Ntrk2, and Grin2b were increased by risperidone and exercise intervention. Exercise upregulated expression of Grin1 and Grin2a. Syn1 and Syp mRNA expression were enhanced by exercise in the risperidone-treated group. The expression of both Mfn1 and Drp1 mRNA were decreased by risperidone-only treatment. In the prefrontal cortex, Bdnf and Dlg4 expression was upregulated by exercise, while the Ntrk2 expression was reduced by risperidone and reversed by exercise. The Mfn1 mRNA expression was decreased by risperidone with or without voluntary exercise. The risperidone-decreased Ppargc1α gene expression was enhanced by exercise.Risperidone affects synaptic plasticity through a complex mechanism in female juvenile rats: enhancing certain key genes in the hippocampus while inhibiting genes essential for mitochondrial function. In line with our hypothesis, voluntary exercise promotes genes beneficial for synaptic plasticity and enhances specific genes reduced by risperidone, in female juvenile rats.Copyright © 2025 The Author(s). Published by Elsevier Inc. All rights reserved.
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