EFFECTS OF MEMANTINE ON NICKEL CHLORIDE INDUCED CEREBELLAR TOXICITY IN WISTAR RATS
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Nickel chloride (NiCl2) is a widespread environmental contaminant that causes neurotoxicity, with the cerebellum showing particular vulnerability due to its central role in motor coordination and high metabolic demands. Memantine, a non-competitive
N-methyl-D-aspartate (NMDA) receptor antagonist. It is hypothesized that its neuroprotective properties could be beneficial in the mitigation of cerebellar damage caused by nickel chloride. This study was aimed at investigating the effects of memantine on the nickel chloride induced cerebellar toxicity in wistar rats. Forty-eight rats were divided into eight groups: Control, nickel chloride only, high dose of memantine + nickel chloride, low dose of memantine + nickel chloride, high dose of memantine, low dose of memantine. The treatment protocol ran for 28 days. A served as control and received 1ml of distilled water daily to compensate for stress of administration, whereas, rats in group B received 2.5mg/kg of NiCl₂, rats in group C received 10mg/kg Og memantine(low dose) and 2.5mg/kg of NiCl₂, rats in group D received 20mg/kg of memantine (high dose) and 2.5mg/kg of NiCl₂, rats in group E received 10mg/kg of memantine (low dose) and rats in group F received 20mg/kg of memantine (high dose). Administration of memantine was done orally using an orogastric tube while the administration of nickel chloride was done via intraperitoneal injection. It lasted for 28days. The body weight of the rats were recorded daily. At the end of the experimental period, the rats were sacrificed by cervical dislocation and the organ( cerebrum) weight was recorded. The parameters accessed include cerebral antioxidant enzymes (SOD, CAT, GPx and GSH), MDA concentration and the histology of the cerebrum using
Hematoxylin and Eosin staining technique. Results obtained showed no significant change (p>0.05) in the initial body weight and final body weight. A significant decrease (p<0.05) was observed in the weight change of rats in group B when compared to control, however, a significant increase (p<0.05) was observed in the weight of groups C and D when compared to group B. No significant change (p>0.05) was observed in the cerebellar and relative cerebellar weight of rats across experimental groups. A significant decrease (p<0.05) was observed in cerebellar SOD, CAT, GPx and GSH activity of rats in group B (2.5 mg/kg bw. NiCl2) when compared to the control. A significant increase (p>0.05) in cerebellar MDA concentrations was observed in the weights of rates in group B (2.5 mg/kg bw. NiCl2 ) when compared with group A. Severe histological alterations in the cerebellum of nickel-chloride exposed rats were observed. However, pre-treatment with memantine mitigated the adverse effects induced by NiCl2. In conclusion, findings from this study shows that memantine exerted antioxidant properties as well as mitigating the histological alterations in the cerebellum.
N-methyl-D-aspartate (NMDA) receptor antagonist. It is hypothesized that its neuroprotective properties could be beneficial in the mitigation of cerebellar damage caused by nickel chloride. This study was aimed at investigating the effects of memantine on the nickel chloride induced cerebellar toxicity in wistar rats. Forty-eight rats were divided into eight groups: Control, nickel chloride only, high dose of memantine + nickel chloride, low dose of memantine + nickel chloride, high dose of memantine, low dose of memantine. The treatment protocol ran for 28 days. A served as control and received 1ml of distilled water daily to compensate for stress of administration, whereas, rats in group B received 2.5mg/kg of NiCl₂, rats in group C received 10mg/kg Og memantine(low dose) and 2.5mg/kg of NiCl₂, rats in group D received 20mg/kg of memantine (high dose) and 2.5mg/kg of NiCl₂, rats in group E received 10mg/kg of memantine (low dose) and rats in group F received 20mg/kg of memantine (high dose). Administration of memantine was done orally using an orogastric tube while the administration of nickel chloride was done via intraperitoneal injection. It lasted for 28days. The body weight of the rats were recorded daily. At the end of the experimental period, the rats were sacrificed by cervical dislocation and the organ( cerebrum) weight was recorded. The parameters accessed include cerebral antioxidant enzymes (SOD, CAT, GPx and GSH), MDA concentration and the histology of the cerebrum using
Hematoxylin and Eosin staining technique. Results obtained showed no significant change (p>0.05) in the initial body weight and final body weight. A significant decrease (p<0.05) was observed in the weight change of rats in group B when compared to control, however, a significant increase (p<0.05) was observed in the weight of groups C and D when compared to group B. No significant change (p>0.05) was observed in the cerebellar and relative cerebellar weight of rats across experimental groups. A significant decrease (p<0.05) was observed in cerebellar SOD, CAT, GPx and GSH activity of rats in group B (2.5 mg/kg bw. NiCl2) when compared to the control. A significant increase (p>0.05) in cerebellar MDA concentrations was observed in the weights of rates in group B (2.5 mg/kg bw. NiCl2 ) when compared with group A. Severe histological alterations in the cerebellum of nickel-chloride exposed rats were observed. However, pre-treatment with memantine mitigated the adverse effects induced by NiCl2. In conclusion, findings from this study shows that memantine exerted antioxidant properties as well as mitigating the histological alterations in the cerebellum.
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