The Role of High-Dose Vitamin A on the Amygdala of Adult Male Wistar Rats Exposed to Toxic Doses of Methamphetamine

Abstract

The amygdala, a major limbic structure, regulates emotional response, anxiety, and memory formation. Methamphetamine is known to trigger oxidative stress and neurodegeneration, whereas vitamin A possesses potent antioxidant properties that may offer neuroprotection. This study evaluated the effect of high-dose vitamin A on the amygdala of adult male Wistar rats exposed to toxic doses of methamphetamine. Twenty (20) adults male Wistar rats were randomly assigned into four groups and received as follows: Group A (control), Group B (METH-only; 5 mg/kg at 3-hours interval within 12 hours in a day), group C (Vitamin A-only; 2.5 mg/kg), while, group D (combined METH 5 mg/kg at 3-hours interval within 12 hours in a day + Vitamin A-only; 2.5 mg/kg). All experimental groups received feed and water. The administration was done orally using intubation method for a period of twenty-eight days. Body weight result revealed a significant reduction in the methamphetamine-only group compared with the control suggesting metabolic disturbance and appetite suppression. Co-treatment with vitamin A improved body weight, indicating a restorative metabolic effect. Biochemical findings showed elevated malondialdehyde (MDA) and decreased glutathione (GSH) and superoxide dismutase (SOD) levels in the methamphetamine group, confirming oxidative damage within the amygdala. Vitamin A treatment markedly reduced MDA and preserved GSH and SOD activities, demonstrating enhanced antioxidant defense. Behavioral testing using the Elevated Plus Maze indicated anxiety-related alterations following methamphetamine exposure, while vitamin A co-administration protected these behavioral changes. Histological results showed that methamphetamine caused neuronal degeneration, vacuolation, and necrosis, whereas vitamin A preserved neuronal integrity and promoted partial structural recovery. In conclusion, high-dose vitamin A significantly mitigated methamphetamine-induced oxidative and structural damage in the amygdala, highlighting its antioxidative and neuroprotective potential against psychostimulant toxicity.