Immunohistochemical studies of codeine medication on the prefrontal cortex and cerebellum of adult Wistar rats

• Main Authors: Victor B. Archibong, Theresa B. Ekanem, Anozeng O. Igiri, Ann M. Lemuel, Ibe M. Usman, Akeem A. Okesina, Nsisong J. Obosi
• Format: Article
• Language: English
• Published: Taylor & Francis Group 2020-01-01
• Series: Cogent Medicine
• Subjects: immunohistochemistry; codeine; prefrontal cortex; cerebellum; astrocytes; wistar rats
• Online Access: http://dx.doi.org/10.1080/2331205X.2020.1824390

Despite the dangers associated with the increased use of prescription opioid drugs, limited researches have addressed the specific effects of prescription opioids on the brain. The objective of this study was to assess the effects of codeine medication on the prefrontal cortex and cerebellum of Wistar rats. The drugs, ArchilinTM with codeine syrup and Dihydrocodeine 30 mg tablets were used for this study. Thirty (30) male Wistar rats were divided into 5 groups labeled A, B, C, D, and E, n = 6. Group A served as control and was given normal saline, group B was treated with 1 mg/kg bodyweight dihydrocodeine, group C was treated with 2 mg/kg bodyweight dihydrocodeine, group D was treated with 2 ml/kg bodyweight ArchilinTM with codeine syrup and group E was treated with 4 ml/kg bodyweight ArchilinTM with codeine syrup. Drugs were administered orally and daily for 21 days. At the end of the treatment period, animals were sacrificed via intraperitoneal injection of ketamine hydrochloride, brains were perfused with phosphate-buffered saline and formal saline before harvested and postfixed in 10% neutral buffered formalin. Sections of the prefrontal cortex and cerebellum were obtained and processed for immunohistochemical studies using GFAP stain. Results from the study suggested that prolonged administration of codeine medication produced an inflammatory reaction in the prefrontal cortex and cerebellum of treatment groups. This neuroinflammatory reaction is an indicator of a pathologic process that could lead to neuronal degeneration, glial degeneration, and altered physiologic process in the prefrontal cortex and cerebellum.