Abstract
Oxycodone (6‐deoxy‐7,8‐dehydro‐14‐hydroxy‐3‐O‐methyl‐6‐oxomorphine) is a semi synthetic opioid. It is most effective for treating patients with post‐surgical, cancer and chronic non‐malignant pain. Recently concern regarding effect of chronic opioid exposure on the development of neuronal degeneration has been emerged. We have investigated induction of biomarkers of brain pathology by chronic oxycodone exposure in rats. We observed significant mitochondrial dysfunction and increase in activated caspase 3 level in brain of rats treated with oxycodone. Recently, it was shown that opioid receptors may be involved in amyloid‐beta production that is one of the characteristics of Alzheimer disease. Thus, we monitored the level of amyloid beta A4 protein. We detected increased accumulation of amyloid beta A4 protein in both nucleus accumbens and cortex areas of oxycodone‐exposed rats. We also observed increase in a‐synuclein level in various brain areas after oxycodone treatment. These data indicates that chronic oxycodone exposure may contribute to premature development of neuronal degeneration in brain areas involved in motivational, memory and executive controls.
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