Mild stress exposure contributes to the development of cognitive and emotional deficits, is considered as a model of depressive state, and is characterized by enhanced NO production. In albino mature (12-month-old) male rats, the depressive state was simulated by daily 30-min exposure to stressful stimuli (vibration, loud sound, and strobe light) over 7 days in a special chamber. On paraffin frontal sections of the brain stained with antibodies against inducible NO synthase (iNOS), the expression and distribution pattern of immunoreactive material were evaluated in various layers of the dentate gyrus under normal conditions and after depression modeling. The relative area of iNOS expression in the dentate gyrus of control rats was 8.2 (7.1-9.9)%, while in rats with experimental depression, this parameter was 16.7 (10.5-22.1)%, i.e. increased by 8.5% (p<0.05). In mature rats with modeled depressive state, the expression and relative area of iNOS expression in neuronal perikarya in the granular and subgranular layers of the dentate gyrus increased, which can underlie the mechanisms of damage and determine reduced neuroplasticity and suppressed neurogenesis in the dentate gyrus in rats during adulthood.
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http://dx.doi.org/10.1007/s10517-020-04963-x | DOI Listing |
J Neurosci Methods
January 2025
Neuroimage Analytics Laboratory and Biggs Institute Neuroimaging Core, Glenn Biggs Institute for Neurodegenerative Disorders, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA; Research Imaging Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA. Electronic address:
Background: The hippocampus plays a crucial role in memory and is one of the first structures affected by Alzheimer's disease. Postmortem MRI offers a way to quantify the alterations by measuring the atrophy of the inner structures of the hippocampus. Unfortunately, the manual segmentation of hippocampal subregions required to carry out these measures is very time-consuming.
View Article and Find Full Text PDFBiochem Biophys Res Commun
December 2024
Laboratory of Exercise Biochemistry and Neuroendocrinology, Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba, Ibaraki, 305-8574, Japan; Division of Sport Neuroscience, Kokoro Division, Advanced Research Initiative for Human High Performance (ARIHHP), Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba, Ibaraki, 305-8574, Japan. Electronic address:
Exercise benefits the brain, particularly the learning and memory center-the dorsal hippocampus (dHPC)-and holds promise for therapeutic applications addressing age-related cognitive deficits. While moderate-to-vigorous-intensity exercise is commonly recommended for health benefits, our translational research proposes the effectiveness of very-light-intensity exercise in enhancing cognitive functions. However, the intensity-dependent characteristics of HPC activation have yet to be fully delineated; therefore, there is no evidence of whether such easily accessible exercises for people of all ages and most fitness levels can activate HPC neurons.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Stevens Neuroimaging and Informatics Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Background: Microglia undergo varying regional dependent functional changes, which can exacerbate cognitive decline in Alzheimer's disease, but the full clinical relevance remains unclear. Ramified microglia survey the micro-environment and inert/amoeboid microglia engulf debris. A third morphological type; rod microglia, have been observed in a number of pathological conditions, but are relatively understudied.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Southern Illinois University School of Medicine, Springfield, IL, USA.
Background: Glutamatergic neurotransmission plays an essential role in learning and memory. Previous studies support a dynamic shift in excitatory signaling with Alzheimer's disease (AD) progression, contributing to negative cognitive outcomes. The majority of previous studies have relied heavily on male physiology when determining these alterations in AD mouse models.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Laboratory of Neuroscience (LIM27), Departamento e Instituto de Psiquiatria, Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, São Paulo, Brazil.
Background: Nearly all individuals with Alzheimer's disease (AD) develop neuropsychiatric symptoms (NPS). Lithium is a mood-stabilizer and is efficient in reducing disruptive behaviors in bipolar-disorder; this characteristic could be an opportunity to investigate the use of lithium in treating behavioral changes in AD.
Method: We tested lithium carbonate treatment in 3xTg-AD and age-matched Wild-type male mice (CEUA/PROCESS: 1605/2020; 4127240122).
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