Changes in rat brain regions serotoninergic system following acephate poisoning

Abstract

Acephate ( O, S-dimethyl acetylphosphoramidothioic acid) is an organophosphate pesticide used throughout the world extensively. Anticholinesterase action of acephate produces cholinotoxicity and may produce compensatory changes in other neurotransmitter levels. The objective of the present investigation was (1) to find brain region specific changes and (2) duration related treatment effects of the organophosphate acephate exposure on serotoninergic system. Reports of repeated exposure to organophosphate pesticide induced changes in rat brain serotoninergic system are limited. The present study analyses changes in 5-hydroxytryptamine (5-HT) level and its metabolite 5-hydroxy indoleacetic acid (5-HIAA) level at 0, 4, 14, and 60 days of oral acephate exposure (178 mg/kg) in the rat brain regions: olfactory lobe, cerebellum, pons, medulla oblongata, spinal cord, hypothalamus, hippocampus, striatum, midbrain, and cortex. Acephate exposure decreased 5-HT level in cortex, hippocampus, striatum, hypothalamus, midbrain, and spinal cord brain regions at the 4, 14, and 60 days durations studied. Duration specific decrease in 5-HT level was observed in olfactory lobe at 4 and 14 days and in pons, medulla oblongata, and cerebellum brain regions at 14 and 60 days of treatment. 5-HIAA levels were decreased in the brain regions cortex, pons, medulla oblongata, and spinal cord at all the durations of treatment studied and in hypothalamus (4 days) and cerebellum (60 days). A short-term increase in 5-HIAA levels was observed in olfactory lobe and midbrain after 14 days of treatment. The results reveal that acephate exposure produced activation of the serotoninergic system and the increased activity of serotoninergic neurons results in decrease of the monoamine levels and its metabolite in brain regions.