This can't be stressed enough: The contribution of select environmental toxicants to disruption of the stress circuitry and response

• Type of Material: Article
• Authors: William Caudle, Emory University
• Language: English
• Date: 2016-11-01
• Publisher: Elsevier
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2015 Elsevier Inc. All rights reserved.
• Final Published Version (URL): http://dx.doi.org/10.1016/j.physbeh.2015.09.021
• Title of Journal or Parent Work: Physiology and Behavior
• ISSN: 0031-9384
• Volume: 166
• Start Page: 65
• End Page: 75
• Grant/Funding Information: Financial support for this work was provided by a pilot grant from the Emory HERCULES Exposome Research Center P30 ES019776 (WMC).
• Keywords: CORTICOTROPIN-RELEASING-FACTOR; Science & Technology; Catecholamines; Psychology, Biological; Behavioral Sciences; GABA; Life Sciences & Biomedicine; DENDRITIC SPINE DENSITY; BASOLATERAL AMYGDALA; AMYGDALA LESIONS BLOCK; Limbic; Social Sciences; Psychology; Glucocorticoids; RAT-BRAIN SYNAPTOSOMES; BISPHENOL-A EXPOSURE; Glutamate; Pesticide; DELTA-HEXACHLOROCYCLOHEXANE ISOMERS; MEDIAL PREFRONTAL CORTEX; LONG-TERM POTENTIATION; PITUITARY-ADRENAL AXIS
• Research Categories: Environmental Sciences; Biology, Neuroscience; Health Sciences, Public Health

Abstract

Integration of the hypothalamic–pituitary–adrenal (HPA) axis and the limbic system through glucocorticoid signaling is imperative in initiating and regulating a suitable stress response following real or perceived threats. Dysfunction of these circuits that results in a persistent or inhibited glucocorticoid secretion can severely affect processing of stressful experiences and lead to risk for developing further psychiatric pathology. Exposure to toxic chemicals found in our environment, including pesticides, metals, and industrial compounds, have been shown to have significant impact on neurological health and disease. Indeed, studies have begun to identify the HPA axis and limbic system as potential targets of many of these environmental chemicals, suggesting a possible environmental risk for damage to the stress circuit and response to stressful stimuli. This review will focus on our current understanding of the impact exposure to environmental toxicants, including bisphenol A and lead, has on the synaptic physiology of the HPA axis and limbic system and how this contributes to an alteration in behavior output. Further, this discussion will provide a starting point to continue to couple novel toxicological and neurological approaches to elaborate our understanding of the influence of environmental chemicals on the stress response and pathology.