ArticleBrain, behavior, and immunity2019
Pyridostigmine bromide and stress interact to impact immune function, cholinergic neurochemistry and behavior in a rat model of Gulf War Illness.
Article in Brain, behavior, and immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Cholinergic stimulation after acute myocardial infarction improves hemodynamic parameters and modulates the renal injury in spontaneously hypertensive rats.Scientific reports · 2026Article
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- Exposing the latent phenotype of Gulf War Illness: examination of the mechanistic mediators of cognitive dysfunction.Frontiers in immunology · 2024Review
- Longitudinal evaluation of structural brain alterations in two established mouse models of Gulf War Illness.Frontiers in neuroscience · 2024Article
- Novel characterization of endogenous transient receptor potential melastatin 3 ion channels from Gulf War Illness participants.PloS one · 2024Article
- Delayed cognitive impairments in a rat model of Gulf War Illness are stimulus-dependent.Brain, behavior, and immunity · 2023Article
- Impact of gulf war toxic exposures after mild traumatic brain injury.Acta neuropathologica communications · 2022Article
- Pyridostigmine bromide elicits progressive and chronic impairments in the cholinergic anti-inflammatory pathway in the prefrontal cortex and hippocampus of male rats.Neurobiology of stress · 2022Article
- Association of the tissue microstructural diffusivity and translocator protein PET in Gulf War Illness.Brain, behavior, & immunity - health · 2021Article
- Gulf War Illness: Mechanisms Underlying Brain Dysfunction and Promising Therapeutic Strategies.Pharmacology & therapeutics · 2021Review
- Cholinergic neurotransmission in the basolateral amygdala during cued fear extinction.Neurobiology of stress · 2020Article
- Assessing the Beneficial Effects of the Immunomodulatory Glycan LNFPIII on Gut Microbiota and Health in a Mouse Model of Gulf War Illness.International journal of environmental research and public health · 2020Article
- Assessment of zebrafish embryo photomotor response sensitivity and phase-specific patterns following acute- and long-duration exposure to neurotoxic chemicals and chemical weapon precursors.Journal of applied toxicology : JAT · 2020Article
- Acetylcholinesterase inhibitor exposures as an initiating factor in the development of Gulf War Illness, a chronic neuroimmune disorder in deployed veterans.Neuropharmacology · 2020Review
- Interactions between pyridostigmine bromide and stress on glutamatergic neurochemistry: Insights from a rat model of Gulf War Illness.Neurobiology of stress · 2020Article
- Neurochemical and neuroinflammatory perturbations in two Gulf War Illness models: Modulation by the immunotherapeutic LNFPIII.Neurotoxicology · 2020Article
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- A permethrin metabolite is associated with adaptive immune responses in Gulf War Illness.Brain, behavior, and immunity · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Gulf War Illness (GWI) is characterized by a constellation of symptoms that includes cognitive dysfunction. While the causes for GWI remain unknown, prophylactic use of the acetylcholinesterase inhibitor pyridostigmine bromide (PB) in combination with the stress of deployment has been proposed to be among the causes of the cognitive dysfunction in GWI. Mechanistically, clinical studies suggest that altered immune function may be an underlying factor in the neurochemical and neurobehavioral complications of GWI. Accordingly, the goal of this study was to determine how responses to an immune challenge (lipopolysaccharide; LPS) or stress impacts inflammation, acetylcholine (ACh) neurochemistry and behavior in an experimental model of GWI. Rats with a history of PB treatment exhibited potentiated increases in C-reactive protein levels in response to a submaximal LPS challenge compared to control rats, indicating that prior treatment with this cholinesterase inhibitor leads to exacerbated inflammatory responses to a subsequent immune challenge. ACh responses to LPS administration were decreased in the hippocampus, but not prefrontal cortex (PFC), in rats with a prior history of PB treatment or stress exposure. Additionally, ACh release in response to acute immobilization stress was attenuated in the PFC and hippocampus in these groups. These attenuated cholinergic responses were accompanied by impairments in contextual and cue-based fear learning. The results of this study suggest that stress and LPS challenges adversely affect central ACh neurochemistry in a rodent model of GWI and support the hypothesis that dysregulated immune responses are mechanistically linked to the neurological complications of GWI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.