The effects of estrogen on carrageenan-induced nociceptive behaviors and inflammatory mediators in ovariectomized female mice
Item
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Title
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The effects of estrogen on carrageenan-induced nociceptive behaviors and inflammatory mediators in ovariectomized female mice
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Identifier
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d_2009_2013:1273edc68305:10529
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identifier
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10847
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Creator
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Abrams, Lisa C.,
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Contributor
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Vanya Quinones-Jenab
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Date
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2010
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Language
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English
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Publisher
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City University of New York.
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Subject
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Physiological psychology | Behavioral psychology | Behaviors | Cytokines | Estrogen | Indomethacin | Inflammation | Mice
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Abstract
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Epidemiological studies have shown that pain perception is sexually dimorphic; females tend to experience greater sensitivity to painful stimuli and more chronic pain compared to males. Researchers believe that this dichotomy is caused by the distinct endocrinological profile of females. 17beta-estradiol has been shown to attenuate inflammatory behaviors in both the formalin and carrageenan (Cg) models of inflammation. Research also shows that estrogen affects many inflammatory mediators, including proinflammatory cytokines and prostaglandins (PG). Estrogen plays an important, yet complicated role, in inflammation, and little is known about the specific biochemical mechanisms involved. The objective of this study is to determine if, similar to rats, estrogen attenuates Cg-induced thermal hyperalgesia by altering cytokine or PG release. To that end, female OVX mice were pretreated with various doses of estradiol and injected with 1% Cg. Paw withdrawal latency was recorded prior to, 1 hour, and 5 hours after Cg-treatment in response to a low, medium, and high heat stimuli. Additional animals were treated with indomethacin, a COX blocker. High doses of estradiol caused an increase in nociceptive responses prior to and subsequent to Cg administration. This increase in these pain behaviors was not directly caused by an increase in proinflammatory cytokine levels or a decrease in anti-inflammatory cytokines levels. However, estradiol caused increases in cytokine levels in the untreated paw. Furthermore, treatment with indomethacin caused an attenuation of hyperalgesia. Additionally, indomethacin negated the difference between estradiol- and vehicle-treated mice, indicating that estrogen may interact with prostanoid synthesis. This effect, however, was not seen in the Cg-treated paw, suggesting that estradiol may be increasing hyperalgesia via another pathway as well. Taken together, our results suggest that estrogen's hyperalgesic effects are partly mediated through cytokine up-regulation and prostanoid synthesis, but the main mechanism of action still needs further investigation.
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Type
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dissertation
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Source
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2009_2013.csv
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degree
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Ph.D.
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Program
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Psychology
