Stress Hormone Enhancement of OP-induced Neuroinflammation as an Animal Model of GWI: The Role of Toll-like Receptors and Plasticity

Abstract

GWI is a multi-symptom disorder with features similar to sickness behavior (e.g., fatigue, depression, cognitive impairments, sleep disturbances, gastrointestinal problems). The exposures and conditions in theater that caused GWI remain unknown but several classes of chemicals and physiological/environmental conditions have been implicated. We are working to expand upon our previously developed mouse model of GWI combining corticosterone (CORT), as a stressor mimic, and DFP, a sarin surrogate. As such, we have tested the combination of chlorpyrifos oxon (CPO) with CORT in our long-term exposure paradigm. However, using the lower dose of CPO being employed in the behavioral experiments did not result in significant neuroinflammation. Additionally, dose response studies are being performed to determine an appropriate dose for dichlorvos that produces neuroinflammation. In year 2, the CORT CPO regimen will be repeated with a higher dose of CPO and dichlorvos will be implemented in the GWI model.

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Document Details

Document Type
Technical Report
Publication Date
Nov 01, 2017
Accession Number
AD1052111

Entities

People

  • James P. O'Callaghan
  • Julie Miller
  • Kimberly A. Kelly
  • Lindsay T. Michalovicz

Organizations

  • Centers for Disease Control and Prevention

Tags

DTIC Thesaurus Topics

  • Acetylcholinesterases
  • Biomedical Research
  • Blood-Brain Barrier
  • Brain
  • Cell Physiological Processes
  • Cells
  • Chemical Synthesis
  • Chemistry
  • Cytoskeleton
  • Diseases And Disorders
  • Governments
  • Medical Personnel
  • Nerve Agents
  • Neurosciences
  • Persian Gulf Syndrome
  • Proteins

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  • Neurotoxicology
  • Psychological Intervention/Treatment for Stress, Anxiety, PTSD, and Related Emotional and Cognitive Health Symptoms.