Objective: To investigate the protective effect of blueberry extract (BE, 25% anthocyanins) against oxidative damage in primary cultures of rat hippocampal neurons induced by H2O2.
Methods: Rat hippocampal neurons were randomly assigned to control group, H2O2 group and BE pretreatment groups, BE at six different doses (0.01, 0.1, 1.0, 10.0, 20.0 and 40 microg/ml) and then exposed to 50 micromol/L H2O2 for twenty-four hours. To selecte the most fittest concentration of BE by testing viability of neurons and activity of LDH. Then MDA concentration, SOD activity and neuronal apoptosis were(checked) measured.
Results: (1) Compared with H2O2 group, the hippocampal cell viabilities in the 0.1, 1.0 and 10 microg/ml BE groups were significantly increased from 57.44% to 78.42%, 87.71% and 72.40% separately. The activity of LDH in BE groups at varied concentrations (0.1, 1.0 and 10 microg/ml) was significiantly lower than that in H2O2 group. It was found that 1 microg/ml BE had the furthest protective effect against oxidative damage in primary cultures of rat hippocampal neurons induced by H2O2. (2) The concentration of MDA and the rate of neuronal apoptosis of BE group (1 microg/ml) were much lower than H2O2 group, while SOD activity was much higher.
Conclusion: Proper dose of BE has remarkable protective effect against oxidative stress in primary cultures of rat hippocampal neurons induced by H2O2, the mechanism may be related to decreasing the neuronal apoptosis and enhancing the antioxidation of hippocampal neurons.
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Brain Behav
January 2025
Department of Psychiatry, Dalhousie University, Halifax, Nova Scotia, Canada.
Introduction: Patients with bipolar disorder (BD) demonstrate episodic memory deficits, which may be hippocampal-dependent and may be attenuated in lithium responders. Induced pluripotent stem cell-derived CA3 pyramidal cell-like neurons show significant hyperexcitability in lithium-responsive BD patients, while lithium nonresponders show marked variance in hyperexcitability. We hypothesize that this variable excitability will impair episodic memory recall, as assessed by cued retrieval (pattern completion) within a computational model of the hippocampal CA3.
View Article and Find Full Text PDFInt J Dev Neurosci
February 2025
Department of Digestive and Nutrition, College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China.
Neonatal hypoxic-ischemic encephalopathy (HIE) is a severe neurological injury during infancy, often resulting in long-term cognitive deficits. This study aimed to investigate the neuroprotective effects of Edaravone (EDA), a free radical scavenger, and elucidate the potential role of brain-derived neurotrophic factor (BDNF) in mediating these effects in neonatal HIE rats. Using the Rice-Vannucci model, HIE was induced in neonatal rats, followed by immediate administration of EDA after the hypoxic-ischemic insult.
View Article and Find Full Text PDFBiol Psychiatry Glob Open Sci
March 2025
Department of Psychiatry, Division of Systems Neuroscience, Columbia University, New York State Psychiatric Institute, New York, New York.
Background: Impairments in behavioral pattern separation (BPS)-the ability to distinguish between similar contexts or experiences-contribute to memory interference and overgeneralization seen in many neuropsychiatric conditions, including depression, anxiety, posttraumatic stress disorder, dementia, and age-related cognitive decline. Although BPS relies on the dentate gyrus and is sensitive to changes in adult hippocampal neurogenesis, its significance as a pharmacological target has not been tested.
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Cureus
December 2024
School of Allied Health Sciences, Manav Rachna International Institute of Research and Studies, Faridabad, IND.
Introduction: Sleep deprivation (SD), stemming from a myriad of aetiologies, is a prevalent health condition frequently overlooked. It typically impairs memory consolidation and synaptic plasticity, potentially through neuroinflammatory mechanisms and adenosinergic signalling. It is still unclear whether the adenosine A1 receptor (A1R) modulates SD-induced neurological deficits in the hippocampus.
View Article and Find Full Text PDFAcetylcholine modulates the network physiology of the hippocampus, a crucial brain structure that supports cognition and memory formation in mammals . In this and adjacent regions, synchronized neuronal activity within theta-band oscillations (4-10Hz) is correlated with attentive processing that leads to successful memory encoding . Acetylcholine facilitates the hippocampus entering a theta oscillatory regime and modulates the temporal organization of activity within theta oscillations .
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