Low arsenic concentrations impair memory in rat offpring exposed during pregnancy and lactation: Role of α7 nicotinic receptor, glutamate and oxidative stress

• Published in: Neurotoxicology (Park Forest South) 2018-07, Vol.67, p.37-45
• Main Authors: Mónaco, Nina María, Bartos, Mariana, Dominguez, Sergio, Gallegos, Cristina, Bras, Cristina, Esandi, María del Carmen, Bouzat, Cecilia, Giannuzzi, Leda, Minetti, Alejandra, Gumilar, Fernanda
• Format: Article
• Language: English
• Subjects: Arsenic; Female rats; Glutamate; Oxidative stress; α7-nicotinic receptor
• ISSN: 0161-813X; 1872-9711
• DOI: 10.1016/j.neuro.2018.04.011

•Exposure to arsenic during development impairs memory in female offspring.•Exposure to arsenic decreases the expression of α7-AChR in hippocampus.•Low arsenic levels cause oxidative damage in whole brain and hippocampus.•Exposure to arsenic increases glutamate levels that may produce excitotoxicity. Inorganic arsenic (iAs) is an important natural pollutant. Millions of individuals worldwide drink water with high levels of iAs. Arsenic exposure has been associated to cognitive deficits. However, the underlying mechanisms remain unknown. In the present work we investigated in female adult offspring the effect of the exposure to low arsenite sodium levels through drinking water during pregnancy and lactation on short- and long-term memory. We also considered a possible underlying neurotoxic mechanism. Pregnant rats were exposed during pregnancy and lactation to environmentally relevant iAs concentrations (0.05 and 0.10 mg/L). In 90-day-old female offspring, short-term memory (STM) and long-term memory (LTM) were evaluated using a step-down inhibitory avoidance task. In addition, we evaluated the α7 nicotinic receptor (α7-nAChR) expression, the transaminases and the oxidative stress levels in hippocampus. The results showed that the exposure to 0.10 mg/L iAs in this critical period produced a significant impairment in the LTM retention. This behavioral alteration might be associated with several events that occur in the hippocampus: decrease in α7-nAChR expression, an increase of glutamate levels that may produce excitotoxicity, and a decrease in the antioxidant enzyme catalase (CAT) activity.