Acute Alloxan Exposure Alters Cortical Oscillatory Power before Sustained Hyperglycemia in Wistar Rats

Alloxan is widely used to induce experimental diabetes mellitus, but acute electrophysiological effects occurring before established hyperglycemia remain insufficiently characterized. We evaluated motor-cortex electrocorticographic (ECoG) activity and blood glucose in adult male Wistar rats after a single intraperitoneal dose of alloxan (150 mg/kg). Six independent cohorts (n = 9 per cohort) comprised an ad libitum-fed control, a 12 h fasting control, and alloxan groups evaluated at 24, 48, 72, or 96 h after administration. Blood glucose decreased markedly at 24 and 48 h and returned toward control values at 72 and 96 h; sustained hyperglycemia was not observed during the 96 h observation window. Alloxan-exposed cohorts showed significant differences in ECoG power, including changes in theta, alpha, beta, and gamma activity. Integrated spectral power across the broader 1–12 Hz (delta–alpha) and 12–40 Hz (beta–gamma) windows also differed among cohorts. These findings establish an acute electrophysiological phenotype temporally associated with alloxan exposure during dysglycemia, but they do not establish direct central nervous system neurotoxicity or a specific mechanism. Blood–brain barrier permeability, oxidative stress, neuroinflammation, histological injury, and brain alloxan concentrations were not measured. Acute postalloxan electrophysiological effects should therefore be considered a potential confounder in neuropharmacological studies using this experimental model.