Chronic exposure to metam sodium causes cognitive impairment in adult mice: evidence of hippocampal neuroinflammation

Abstract

Neuroinflammation is a significant pathological feature contributing to cognitive deficits that can arise from exposure to environmental toxicants such as pesticides. Metam sodium (MS) is one of the emergent pesticides largely used in the agriculture and public health sectors. In the present study, we verified whether exposure to this compound would affect cognitive performance, and induce neuroinflammation as an underlying mechanism. In this context, mice received chronic treatment with different doses of MS and were submitted to novel object recognition and step-through passive avoidance tests. Hippocampal regions from treated animals underwent an immunohistochemical evaluation of the expression of GFAP and Iba-1 as markers of astrocytes and microglia respectively. The main findings showed that chronic exposure to MS resulted in a decrease in the ratio of time spent beside the novel object and strep-through latency indicating alterations in recognition memory as well as short- and long-term memory respectively. Moreover, treated animals exhibited a significant rise in immunostaining of neuroinflammatory markers GFAP and Iba-1 in the dentate gyrus as well as in the CA1 and CA3 areas of the hippocampus. The present work demonstrates that MS diminished cognitive performance in tasks relying on hippocampal-dependent memory closely associated with high expression of neuroinflammatory markers.
 Keywords: Metam sodium; cognitive performance; neuroinflammation; hippocampus; GFAP; Iba-1.