Characterization of the Increased Risk of Attention Deficit Hyperactivity Disorder Following Early-Life Exposure to Deltamethrin
Unmasking the mechanistic etiology of neurodevelopmental disorders remains at the forefront of neuroscience research. To this end, epidemiological studies have sought to identify key risk factors driving these disorders. Unsurprisingly, early-life exposure to ubiquitous pesticides which target the central nervous system has been identified as one such risk factor. Pyrethroids, a popular class of insecticides, have been directly correlated with an increased risk in Attention Deficit Hyperactivity Disorder (ADHD). The focus of this thesis is to elucidate the mechanism through which the pyrethroid deltamethrin (DM) contributes to the development of ADHD. Our studies identify perturbations in voltage-gated sodium (Nav) channel 1.6 and medium spiny neurons which highly express Nav1.6- both of which are key components of reward circuitry. These studies are further complemented by identification of behavioral aberrations that typify the human pathophysiology of ADHD. Together, this data identifies a possible mechanism through which early-life exposure to DM disrupts reward circuitry contributing to the etiology of ADHD.