Atrazine-Induced Hippocampal Degeneration and Behavioral Deficits in Wistar Rats: Mitigative Role of Avocado Oil

Abstract

Background: Glutamate is essential to learning and memory as an excitatory neurotransmitter. This study evaluated the atrazine effect on the hippocampus and examined the mitigative role of avocado oil against the neuronal degeneration and behavioral deficits in Wistar rats. Methods: Fifty adult male Wistar rats were divided into four groups of ten. Group 1 (controls) received 0.5 ml distilled water; group 2 received atrazine (215 mg/kg/d); group 3 received avocado oil (1 ml/ 250 g/d); group 4 received avocado oil (1 ml/ 250 g/d) 60 minutes before atrazine. Treatments were given by oral gavage over 28 days. Barnes maze and Y-maze tests were performed to assess the learning and memory. Histological and Glial Fibrillary Acidic Protein (GFAP)-immuno-reaction in the hippocampus were assessed, using Hematoxylin and Eosin (H&E) stain and anti-GFAP antibody. The glutamate and acetylcholinesterase levels were subsequently assessed. Results: The learning and memory performance was significantly affected in group 2, but improved in group 4. In group 3, learning and memory performance was not different from group 1. In group 2, atrazine caused massive neurodegeneration and astrogliosis at Cornu Ammonis-1 (CA-1) and Dentate Gyrus (DG). Combined avocado and atrazine significantly reduced neuronal death and astrogliosis in CA-1 and DG areas. In group 2, glutamate level was high while acetylcholinesterase was low. In group 4, glutamate was low but acetylcholinesterase was high compared to those in group 2. Glutamate and acetylcholinesterase levels in group 3 was not significantly different from that of group 1. Conclusion: Atrazine inhibited acetylcholinesterase and induced glutamate release. These were associated with excitotoxicity and neuronal degeneration in CA-1 and DG areas as shown by poor learning and memory. Treatment with avocado oil protected against high glutamate release, thus, mitigating neuronal degeneration and maintaining normal learning and memory in rats.