This lab uses multiple techniques to assess the neurotoxicity and behavioral toxicity, associated with environmental chemical exposures, including both operant and spontaneous behaviors, immunohistochemistry, western blotting enzyme linked immunosorbent assays, high-performance liquid chromatography for central neurotransmitter quantification, histology, unbiased stereology, histological imagine analysis, and many others, as means of identifying neurotoxicity of environmental toxicants and non-chemical stressors. Neurotoxicity is examined concomitantly with the assessment of behavioral function. We emphasize behavioral endpoints that can be used across species to facilitate interpretation and direct translation to human populations, This lab examines behaviors across multiple domains including motor function/coordination, response control, fear/anxiety-like behavior, attention, learning, memory, startle response, and social behavior.
Enhanced Neurotoxicity of Metals in Combination With Other Pertinent Risk Factors
The potential synergistic neurodevelopmental consequences of developmental lead exposure in conjunction with maternal and/or offspring stress. Determination of whether enhanced toxicity of lead exposure and stress is seen with other neurotoxic metals, including methylmercury and arsenic, that likewise impact the HPA axis and brain mesocorticolimbic systems. The potential for positive vs negative early behavioral experience to modify the trajectory of consequences of developmental lead and/or prenatal stress exposures.
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The Impact of Developmental Air Pollution (Ultrafine Particle) Exposure on the Brain
The role of developmental air pollution as a risk factor for autism and/or schizophrenia phenotypes. The basis for sex differences in male specific brain vulnerability to developmental air pollution exposures.
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Lead and Prenatal Stress Associated Epigenetic Alterations
Can early behavioral experience alter lead and or prenatal stress induced epigenetic alterations in frontal cortex and hippocampus?
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Can low doses of estrogenic chemicals, that each produce common adverse effects, act together via downstream physiological targets to produce enhanced neurotoxicity, manifest in behavior and corresponding neuroendocrine mediating pathways?
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