Dysregulation of Retinal Melatonin Biosynthetic Pathway and Differential Expression of Retina-Specific Genes Following Blast-Induced Ocular Injury in Ferrets

Neurology International, Journal Year: 2025, Volume and Issue: 17(3), P. 42 - 42

Published: March 17, 2025

Background/Objectives: Blast-induced traumatic ocular injuries (bTOI) pose a significant risk to military and civilian populations, often leading visual impairment or blindness. Retina, the innermost layer of tissue consisting photoreceptor glial cells, is highly susceptible blast injuries. Despite its prevalence, molecular mechanisms underlying retinal damage following bTOI remain poorly understood, hindering development targeted therapies. Melatonin, neuroprotective indoleamine with antioxidant, anti-inflammatory, circadian regulatory properties, synthesized in retina plays crucial role health. Similarly, retina-specific genes, such as Rhodopsin, Melanopsin, RPE65, are essential for function, signaling, cycle. However, their responses exposure have not been thoroughly investigated. Methods: In this study, we utilized ferret model evaluate temporal expression melatonin-synthesizing enzymes, tryptophan hydroxylase 1 2 (TPH1 TPH2), Aralkylamine N-acetyltransferase (AANAT), Acetylserotonin-O-methyltransferase (ASMT), genes (Rhodopsin, Melanopsin) pigment epithelium-specific 65 kDa protein (RPE65) at 4 h, 24 7 days, 28 days post-blast. Ferrets were exposed tightly coupled overpressure waves using an advanced simulator, tissues collected quantitative polymerase chain reaction (qPCR) analysis. Results: The results revealed dynamic multiphasic transcriptional responses. TPH1 TPH2 exhibited upregulation followed by downregulation indicating blast-induced dysregulation metabolism, including melatonin synthesis. AANAT ASMT showed acute post-blast, late-phase disruptions. Rhodopsin increased h but declined while Melanopsin RPE65 demonstrated early downregulation, reflecting potential disruptions regulation Conclusions: These findings highlight complex bTOI, involving neuroinflammation, oxidative stress, synthesis cell functions. emphasize therapeutic mitigating preserving function.

Language: Английский

Serotonin drives aggression and social behaviors of laboratory male mice in a semi-natural environment

Frontiers in Behavioral Neuroscience, Journal Year: 2024, Volume and Issue: 18

Published: Sept. 18, 2024

Aggression is an adaptive social behavior crucial for the stability and prosperity of groups. When uncontrolled, aggression leads to pathological violence that disrupts group structure individual wellbeing. The comorbidity uncontrolled across different psychopathologies makes it a potential endophenotype mental disorders with same neurobiological substrates. Serotonin plays critical role in regulating impulsive aggressive behaviors. Mice lacking brain serotonin, due ablation tryptophan hydroxylase 2 (TPH2), rate-limiting enzyme serotonin synthesis, could serve as model studying aggression. Home cage monitoring allows continuous observation quantification non-social behaviors group-housed, freely-moving mice. Using ethological approach, we investigated impact central on everyday expression their correlations undisturbed, group-living

Language: Английский

Functional study of residual iCre activity relevant for split-Cre applications

Current Research in Biotechnology, Journal Year: 2024, Volume and Issue: unknown, P. 100263 - 100263

Published: Oct. 1, 2024

Language: Английский