Ascorbic Acid Supplementation Improves Adolescent Stress-induced Cognitive Impairment Through Restoration of Behavioral, Biochemical and Electrophysiological Alterations in Male Rats

• Published in: Neuroscience 2024-06, Vol.549, p.55-64
• Main Authors: Ghasemi, Sima Gul, Khoshrou, Alireza, Kakhki, Samaneh, Shirinzadeh Feizabadi, Atefeh, Masoudi, Maha, Bagherifar, Faezeh, Beheshti, Farimah
• Format: Article
• Language: English
• Subjects: Adolescent; Animals; Antioxidants - pharmacology; Ascorbic acid; Ascorbic Acid - pharmacology; Avoidance Learning - drug effects; Brain-Derived Neurotrophic Factor - metabolism; Chronic mild stress; Cognitive Dysfunction - drug therapy; Cognitive Dysfunction - etiology; Cognitive Dysfunction - metabolism; Dietary Supplements; Hippocampus - drug effects; Hippocampus - metabolism; Ki67; Male; Maze Learning - drug effects; Maze Learning - physiology; Memory impairment; Neuronal Plasticity - drug effects; Neuronal Plasticity - physiology; Oxidative Stress - drug effects; Oxidative Stress - physiology; Rats; Rats, Wistar; Stress, Psychological - drug therapy; Stress, Psychological - metabolism
• ISSN: 0306-4522; 1873-7544; 1873-7544
• DOI: 10.1016/j.neuroscience.2024.04.012

[Display omitted] •Chronic Unpredictable mild stress (CUMS) increased serum Corticosterone level.•UCMS increased oxidative stress status and neuro-inflammation and decreasing BDNF and Ki67 in the brain.•Oxidative stress and neuro-inflammation followed by learning and memory impairment in adolescent male rats.•Ascorbic acid (AA) improved learning and memory impairment.•Vit C decreased serum corticosterone level, brain oxidative stress damage and increased BDNF and neurogenesis. The present research study aimed to investigate the role of Ascorbic acid (AA) on synaptic plasticity, learning, and memory impairment induced by unpredicted chronic mild stress (CUMS) in adolescent male rats. Adolescent male rats were divided into: 1) vehicle, 2) CUMS, 3–5) CUMS plus various doses of AA by oral gavage (CUMS-10/100/400 mg/kg), and 6) AA400 mg/kg by oral gavage. In Morris Water Maze, the time latency decreased, while the time spent in the target quadrant increased in CUMS group treated with AA at the dose of 400 mg/kg. In passive avoidance, the latency of entering into the dark chamber decreased in CUMS group treated with AA (400 mg/kg). In biochemical test results, nitrite and MDA significantly decreased, while thiol content, SOD, and catalase activity in CUMS group that received AA400mg/kg was increased. IL-10, BDNF and Ki67 increased, while TNF-a and AChE activity were decreased in CUMS group treated with AA simultaneously. The results of our study showed that chronic stress during adolescence could cause learning and memory disorders as well as synaptic plasticity. In addition, we showed that AA can prevent this problem by reducing oxidative stress, inflammation, increasing the amount of BDNF, and neurogenesis.