Post-traumatic stress disorder (PTSD) is a serious psychiatric disorder characterized by hyper-response to environmental cues as well as the associated depressive and cognitive dysfunctions. According to the key roles of hippocampus for cognitive and emotional regulation, improving hippocampal functions, particularly hippocampal neural plasticity, is the necessary pathway to attenuate the core symptoms of PTSD. The effects of the alternative therapies such as exercise and natural compounds to reduce PTSD symptoms and promote adult hippocampal neurogenesis have been widely demonstrated. However, what is the effect of combining the exercise with traditional Chinese medical compounds remains unknown. In current study, we evaluated the effects of catalpol, which showed the pro-neurogenic effects in previous report, in regulating exercise-mediated PTSD therapeutic effects. With behavioral tests, we found that catalpol treatment promoted the effects of exercise to reduce the response of mice to dangerous cues, and simultaneously enhanced the antidepressant and cognitive protection effects. Moreover, by immunofluorescence we identified that catalpol promoted exercise-mediated hippocampal neurogenesis by enhancing the neural differentiation and mature neuronal survive. We further found that the promote effects of catalpol to exercise-induced environmental hyper-response, antidepressant effects and cognitive protective effects were all compromised by blocking neurogenesis with temozolomide (TMZ). This result indicates that hippocampal neurogenesis is prerequisite for catalpol to promote exercise-mediated brain functional improvement in PTSD model. In conclusion, our research identified the new function of natural compounds catalpol to promote the exercise-mediated brain functional changes in PTSD model, which depend on its effect promoting adult hippocampal neurogenesis.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8351689 | PMC |
http://dx.doi.org/10.18632/aging.203313 | DOI Listing |
EMBO Rep
January 2025
Center for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, University of Lausanne, Prilly, Switzerland.
Hierarchy provides a survival advantage to social animals in challenging circumstances. In mice, social dominance is associated with trait anxiety which is regulated by adult hippocampal neurogenesis. Here, we test whether adolescent hippocampal neurogenesis may regulate social dominance behavior in adulthood.
View Article and Find Full Text PDFCureus
December 2024
Department of Physiology, Touro College of Osteopathic Medicine, Middletown, USA.
Down syndrome (DS) is a genetic intellectual disorder caused by trisomy of chromosome 21 (Hsa21) and presents with a variety of phenotypes. The correlation between the chromosomal abnormality and the resulting symptoms is unclear, partly due to the spectrum of impairments observed. However, it has been determined that trisomy 21 contributes to neurodegeneration and impaired neurodevelopment resulting from decreased neurotransmission, neurogenesis, and synaptic plasticity.
View Article and Find Full Text PDFNeurosci Lett
January 2025
Department of Pharmacology, School of Pharmacy, International University of Health and Welfare, 2600-1 Kitakanemaru, Ohtawara, Tochigi 324-8501, Japan. Electronic address:
Disruption of gut microbiota balance is known to contribute to the development of anxiety; however, it remains unclear whether dysbiosis-induced anxiety involves the glycogen synthase kinase-3β (GSK-3β)/cAMP response element binding protein (CREB)/brain-derived neurotrophic factor (BDNF) pathway and neurogenesis in the ventral hippocampal dentate gyrus (DG). In this study, Male ddY mice were administered an antibacterial cocktail to induce dysbiosis. The dysbiosis model displayed anxiety-like behaviors in the hole-board and elevated plus-maze tests, decreased the phosphorylation levels of GSK-3β (Ser9) and CREB, decreased the expression level of BDNF in the ventral hippocampus, and reduced neurogenesis in the ventral hippocampal DG.
View Article and Find Full Text PDFPsychoradiology
December 2024
Department of Neurology, the First Hospital of Anhui Medical University, Hefei 230022, China.
Background: The hippocampus has been widely reported to be involved in the neuropathology of major depressive disorder (MDD). All the previous researches adopted group-level hippocampus subregions atlas to investigate abnormal functional connectivities in MDD in absence of capturing individual variability. In addition, the molecular basis of functional impairments of hippocampal subregions in MDD remains elusive.
View Article and Find Full Text PDFCNS Neurosci Ther
January 2025
Beijing Key Laboratory of Hypoxia Translational Medicine, Xuanwu Hospital, Center of Stroke, Beijing Institute of Brain Disorder, Capital Medical University, Beijing, China.
Objective: Ischemia-reperfusion of the abdominal aorta often results in damage to distant organs, such as the heart and brain. This cellular heterogeneity within affected tissues complicates the roles of specific cell subsets in abdominal aorta occlusion model (AAO) injury. However, cell type-specific molecular pathology in the hippocampus after ischemia is poorly understood.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!