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Histological study of the prefrontal cortex of adult wistar rat exposed to primidone (mysoline)

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Obiora O., Onyilo P., Onyekachi I. C.
World News of Natural Sciences
|
2025
|
vol. 63
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issue 2
205-213
EN
Epilepsy is a chronic neurological disorder that often requires long-term administration of antiepileptic drugs (AEDs). Primidone (Mysoline), a first-generation barbiturate-type AED, remains widely prescribed for seizure control and essential tremor. Despite its clinical efficacy, prolonged use of Primidone has been associated with metabolic and neurochemical alterations that could influence cortical function. This study investigated the histological and biochemical effects of Primidone on the prefrontal cortex of adult female Wistar rats. Fifteen healthy rats weighing between 130 and 200 g were randomly divided into three groups of five each: control, low-dose (75 mg/kg), and high-dose (150 mg/kg). The control group received standard feed and water, while the treated groups were administered oral doses of Primidone daily for twenty-eight days. At the end of the exposure period, the rats were sacrificed under anesthesia, and their prefrontal cortices were excised for histological and biochemical analyses. Hematoxylin and eosin staining revealed no significant histoarchitectural alterations or neuronal degeneration across treatment groups compared with the control. However, biochemical assays demonstrated a dose-dependent reduction (p < 0.05) in the activities of key antioxidant enzymes—superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and acetylcholinesterase (AChE)—alongside a marked elevation in malondialdehyde (MDA), an indicator of lipid peroxidation and oxidative stress. These findings suggest that chronic Primidone exposure may impair endogenous antioxidant defense systems in the prefrontal cortex, thereby predisposing neuronal tissues to oxidative injury even in the absence of overt histological damage. The study highlights the need for cautious long-term use of barbiturate-based anticonvulsants and underscores the potential benefits of adjunct antioxidant therapy in mitigating drug-induced neurotoxicity.
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