Abstract
Exposure to traffic-related air pollution (TRAP) is associated with a range of neurodevelopmental disorders in human populations. In rodent models, prenatal TRAP exposure increased depressive behaviors and increased brain microglial activity. To identify cellular mechanisms, we examined adult neurogenesis and the blood–brain barrier (BBB) in relation to cognition and motivated behaviors in rats that were exposed to a nano-sized TRAP subfraction from gestation into adulthood. At age 5 months, exposed male rats had 70% fewer newly generated neurons in the dentate gyrus (DG) of the hippocampus. Microglia were activated in DG and CA1 subfields (35% more Iba1). The BBB was altered, with a 75% decrease of the tight junction protein ZO-1 in the CA1 layer, and twofold more iron deposits, a marker of microhemorrhages. The exposed rats had impaired contextual memory (novel object in context), reduced food-seeking behavior, and increased depressive behaviors (forced swim). Deficits of de novo neurogenesis were inversely correlated with depressive behavior, whereas increased microbleeds were inversely correlated with deficits in contextual memory. These findings give the first evidence that prenatal and early life exposure to TRAP impairs adult hippocampal neurogenesis and increases microbleeds in association with behavioral deficits.
Highlights
Traffic-related air pollution (TRAP) is a ubiquitous environmental health hazard, with increasingly recognized neurodevelopmental effects
Blood–brain barrier (BBB) leakage and microglial activation were indicated for a small sample of young adults exposed to severe air pollution in Mexico City[12]
We examined hippocampal de novo adult neurogenesis together with microglial activation, BBB tight junction marker zona occludens protein 1 (ZO-1), iron deposition, and hippocampal-dependent behaviors
Summary
Traffic-related air pollution (TRAP) is a ubiquitous environmental health hazard, with increasingly recognized neurodevelopmental effects. Gestational TRAP exposure alters cognitive development, delays myelination, and increases anxiety and depressive behaviors[1,2,3,4]. Autism spectrum disorders are associated with increased by elevated TRAP exposure during pregnancy and early postnatal life[5,6,7]. Rodent models of gestational or early postnatal TRAP exposure show impaired object. Because depressive behavior is correlated with de novo neurogenesis[11], we hypothesized that prenatal and early life TRAP exposure would impair hippocampal neurogenesis and hippocampal-dependent behavior, in association with increased brain inflammatory responses. Blood–brain barrier (BBB) leakage and microglial activation were indicated for a small sample of young adults exposed to severe air pollution in Mexico City[12]. Microglia were activated in white matter and hippocampal regions in 2month-old offspring from TRAP-exposed mothers[8]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
