{"id":{"repo_id":"utmb","oai_identifier":"oai:utmb-ir.tdl.org:2152.3/12198"},"canonical_url":"https://search.dev.ndltd.org/etd/utmb/oai:utmb-ir.tdl.org:2152.3/12198","repository":{"repo_id":"utmb","name":"University of Texas Medical Branch","base_url":"https://utmb-ir.tdl.org/server/oai/request"},"display":{"title":"Characterization of the Increased Risk of Attention Deficit Hyperactivity Disorder Following Early-Life Exposure to Deltamethrin","abstract":"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.","abstract_html":"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.","abstract_has_math":false,"creators":["Tapia, Cynthia Marie"],"institution":"The University of Texas Medical Branch at Galveston","degree_name":"Pharmacology and Toxicology (Doctoral)","degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2020,"date_issued":"August 2020","date_published":"August 2020","updated_at":"2026-07-24T05:50:54Z","subjects":["Biology, Neuroscience","Health Sciences, Toxicology"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://hdl.handle.net/2152.3/12198","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Tapia, Cynthia Marie"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2023-12-05T15:19:31Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2023-12-05T15:19:31Z"]},{"key":"dc:date.issued","label":"Date","values":["August 2020"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Pharmacology and Toxicology (Doctoral)"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["The University of Texas Medical Branch at Galveston"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Neuroscience","Health Sciences, Toxicology"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://hdl.handle.net/2152.3/12198"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["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."]},{"key":"dc:format.mimetype","label":"Dc Format Mimetype","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Characterization of the Increased Risk of Attention Deficit Hyperactivity Disorder Following Early-Life Exposure to Deltamethrin"]}]}],"canonical_facts":{"dc:creator":["Tapia, Cynthia Marie"],"dc:date.accessioned":["2023-12-05T15:19:31Z"],"dc:date.available":["2023-12-05T15:19:31Z"],"dc:date.issued":["August 2020"],"dc:description.abstract":["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."],"dc:format.mimetype":["application/pdf"],"dc:identifier.uri":["https://hdl.handle.net/2152.3/12198"],"dc:subject":["Biology, Neuroscience","Health Sciences, Toxicology"],"dc:title":["Characterization of the Increased Risk of Attention Deficit Hyperactivity Disorder Following Early-Life Exposure to Deltamethrin"],"dc:type":["Thesis"],"thesis:degree_name":["Pharmacology and Toxicology (Doctoral)"],"thesis:institution_name":["The University of Texas Medical Branch at Galveston"]},"updated_at":"2026-07-24T05:50:54Z"}