Javier Del Pino received his PharmD degree at the University Complutense University of Madrid in 2004. He has two Master’s in Sciences degrees, 2009 and 2010. He specialized in Neurotoxicology and Neurodevelopmental Toxicology and received his PhD in Toxicology in 2009. In 2010, he worked in Institute of Health Carlos III in the National Center of Environmental Health. From 2010 to 2012, he was Associated Researcher at University of Massachusetts UMASS) working in Sandra Petersen´s Lab in a National Institute of Health (NIH) project on developmental effects of TCDD endocrine disruptor on sexual differentiation. In 2016, he got a position as Associated Professor of Toxicology at the Complutense University of Madrid.

Formamidine pesticides have been described to induce permanent effects on development of monoaminergic neurotransmitters systems. The mechanisms that induce these effects are not known but it has been suggested that these effects could be related to monoamino oxidase (MAO) inhibition. Chlordimeform is a formamidine pesticide which is a very weak inhibitor of MAO, although it has been also described to produce neurodevelopmental toxicity. The effects of maternal exposure to chlordimeform on brain region serotonin levels of male and female off spring rats at 60 days of age were evaluated. Maternal and off spring body weight, physical and general activity development were unaffected by the exposure of dams to chlordimeform (5 mg/kg bw, orally on days 6–21 of pregnancy and 1–10 of lactation). Male and female off spring were sacrificed at 60 days of age and possible alterations in the content and metabolism of 5-HT was determined in brain regions by HPLC. Th e results showed that this neurotransmitter system was altered in a brain regional-related manner. In male and female off spring, chlordimeform induced a significant decrease in the striatum and prefrontal cortex 5-HT and its metabolite 5-HIAA levels. Th is effect was with statistical distinction of sex in the prefrontal cortex. In contrast, chlordimeform caused an\r\nincrease in 5-HT and 5-HIAA content in the hippocampus in male and female off spring with sex interaction. Chlordimeform evoked increase in 5-HT turnover in the prefrontal cortex and hippocampus from females and males respectively but evoked a decrease in these regions from males and females respectively. The present findings indicated that maternal exposure to chlordimeform altered serotonergic neurochemistry in their off spring in prefrontal cortex, striatum and hippocampus, and those variations show that other mechanisms, different from MAO inhibition, are implicated.

Javier Del Pino received his PharmD degree at the University Complutense University of Madrid in 2004. He has two Master’s in Sciences degrees, 2009 and 2010. He specialized in Neurotoxicology and Neurodevelopmental Toxicology and received his PhD in Toxicology in 2009. In 2010, he worked in Institute of Health Carlos III in the National Center of Environmental Health. From 2010 to 2012, he was Associated Researcher at University of Massachusetts UMASS) working in Sandra Petersen´s Lab in a National Institute of Health (NIH) project on developmental effects of TCDD endocrine disruptor on sexual differentiation. In 2016, he got a position as Associated Professor of Toxicology at the Complutense University of Madrid.

Cadmium is an environmental pollutant, which is a cause of concern because it can be greatly concentrated in the organism causing severe damage to a variety of organs including the nervous system, which is one of the most affected. Cadmium is a neurotoxic compound which induces cognitive alterations similar to those produced by Alzheimer’s disease(AD). However, the mechanism through which cadmium induces this effect remains unknown. In this regard, cholinergic system in central nervous system (CNS) is implicated on learning and memory regulation, and it has been reported that cadmium can affect cholinergic transmission and it also induces a more pronounced cell death on cholinergic neurons from basal forebrain, which may explain cadmium effects on learning and memory processes. According to all above, an alteration of cholinergic\r\ntransmission in basal forebrain cholinergic neurons, may result in the cognitive disorders observed after cadmium exposures. The present study is aimed at researching the selective neurotoxicity induced by cadmium on cholinergic system in CNS. For this purpose we evaluated, in basal forebrain region, the cadmium toxic effects on cholinergic transmission in NS56 cholinergic murine septal cell line. This study proves that cadmium induces an alteration of Ach levels and acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) activities in SN56 cells. The alteration of Ach levels was independent of alteration of AChE activity, but dependent of ChAT activity reduction. Our present results provide new understanding of the mechanisms contributing to the harmful effects of cadmium on cholinergic neurons and suggest that cadmium could mediate the cognitive disorders through alteration of cholinergic transmission.