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The effects of methylmercuric chloride exposure on immediate early gene induction in the murine brain
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Cooper, Joel F.. The effects of methylmercuric chloride exposure on immediate early gene induction in the murine brain. Retrieved from https://doi.org/doi:10.7282/T3BZ66CJ

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Uniform TitleThe effects of methylmercuric chloride exposure on immediate early gene induction in the murine brain
NameCooper, Joel F. (author); Kusnecov, Alexander (chair); Reuhl, Kenneth (internal member); Wagner, George (internal member); Zhou, Renping (internal member); Shi, Yufang (internal member); Rutgers University; Graduate School - New Brunswick
Date Created2008
Other Date2008-05 (degree)
SubjectToxicology, Methylmercury--Physiological effect, Mice, Mice--Effects of chemicals on
Extentxv, 204 pages
DescriptionThe present set of experiments was designed to examine the effects of dose, route of administration, and frequency of MeHg exposure on activation of neural stress nuclei, altered behavior in the open field and splenic cytokine production. MeHg exposure is associated with gross neuropathological alterations, behavioral deficits, and suppressed function of the immune system. Results from these experiments show that acute IP and ICV exposure of C57BL6J mice to MeHg results in increased recruitment of stress-associated nuclei, as measured by c-Fos immunoreactivity. Acute IP MeHg administration also causes dose-dependent decreases in exploratory behavior. Peripheral stimulation of the gastrointestinal vagus nerve by acute doses of MeHg could be responsible for stimulation of brainstem nuclei and activation of central stress nuclei, as peripheral exposure to LPS in vagotomized mice results in attenuated c-Fos response in limbic and autonomic regions of the murine brain. Proposed malaise-induced alterations in exploratory behavior may also be linked to vagal activation. In Experiment 2, multiple exposures to MeHg resulted in activation of fewer neural stress nuclei and attenuation of the dose-dependent effects of MeHg on open field behavior noted in Experiment 1. Repeated MeHg treatment followed by exposure to LPS resulted in a significantly increased c-Fos response, demonstrating that the reduction in c-Fos noted in response to repeated MeHg was not due to altered protein synthesis, but more likely due to habituated effects on neurotransmission. The splenic cytokine response to acute MeHg did not significantly affect proinflammatory cytokine production, but did increase IL-2; an effect that could have resulted from T-cell proliferation. Repeated exposure to MeHg increased splenic TNF- α, IL-6 and IL-10 levels, through unknown mechanisms. However, the spleen, which functions to both monitor the circulatory system for immunological stimuli and is the central site for the reticuloendothelial immune system, could be increasing cytokine production through macrophage-induced T-cell activation. Methylmercury has been shown in this thesis to uniquely activate stress-associated nuclei in the murine brain, inhibit exploratory behavior in the open field and increase splenic cytokine production likely due to its documented effects on both the nervous and immune systems.
NotePh.D.
NoteIncludes bibliographical references (p. 171-202).
Genretheses, ETD doctoral
Persistent URLhttps://doi.org/doi:10.7282/T3BZ66CJ
LanguageEnglish
CollectionGraduate School - New Brunswick Electronic Theses and Dissertations
Organization NameRutgers, The State University of New Jersey
RightsThe author owns the copyright to this work.
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