dichlorvos induced ache inhibition in discrete brain regions and the neuro-cognitive implications: ameliorative effect of nigella sativa

Background: there has been a rise in accidental poisoning cases resulting from the indiscriminate use and exposure to dichlorvos (ddvp), especially in developing countries, and no antidote with satisfactory efficacy is currently available. thus, we investigated the ache reactivation potential of nigella sativa oil (nso) following ddvp induced ache inhibition patterns in the brain and the associated cognitive implications.methods: fourty wistar rats were randomly divided into four groups of 10 each.; the controls were administered pbs (1 ml/kg); ddvp (8.8 mg/kg) was given to the experimental group i; while ddvp+nso (8.8 mg/kg + 1 ml/kg) and nso (1 ml/kg) was administered orally to the experimental groups ii and iii respectively. all treatments lasted for 14 consecutive days. morris water maze (mwm) paradigm was used to assess the working memory, then rats were euthanized, the brain excised, three brains were fixed for histological examination (nissl staining), and the other seven brains were homogenized for ache activity and ca^2+ concentrations. data were analyzed statistically, using anova method and p values of ≤0.05 was considered as significant. results: in this study, ddvp differentially inhibited ache activities in various brain regions: cerebellum (86.1%), hippocampus (40.6%), frontal cortex (33.2%), medulla (21.5%), spinal cord (14.8%), and occipital cortex (8.9%). it reduced ca^2+ concentration, but had no effect on the delayed escape latency in the mwm, nor impaired the neuro-architectures. nso caused increased ache activities, ca^2+ concentration and reduced escape latency, and improved histologic architectures. conclusion: we concluded that nso reactivated ddvp-induced ache inhibition and improved memory indices, thus, it may serve as a potential treatment in the management of ddvp poisoning cases.