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Journal of Undergraduate Research

Keywords

estrogen signaling, migraine, pathogenesis, ERβ, estrogen receptor β

College

Physical and Mathematical Sciences

Department

Chemistry and Biochemistry

Abstract

Migraine is a disorder that can include aura, headache, nausea, and hypersensitivity to all sensory modalities. It affects over thirty million people in the US. Migraines affect men and women equally until puberty, but overall migraines affect 3x more women than men. They also increase in frequency and severity during periods of estrogen fluctuation and often subside after menopause. Moreover, hormone supplements and birth control can affect migraine patterns. These correlations of migraine episodes to the menstrual cycle and increased pain sensitivity in response to estrogen suggest that differences in estrogen signaling contribute to migraine. We hypothesized that estrogen receptor β (ERβ) is involved migraine pathogenesis. We determined whether deletion of ERβ causes decreased pain sensitivity in mice after a migraine trigger. To do this, we injected ERβ knockout mice with a common migraine trigger, nitroglycerin. We then determined thresholds for detection of thermal stimulus. In addition, we have measured thresholds to induce aura in ERβ knockout mice. Our preliminary results indicate that ERβ knockout mice do exhibit decreased sensitivity to thermal stimuli compared to wild type siblings after administration of nitroglycerin. This confirms our hypothesis that estrogen receptor signaling is part of migraine pathogenesis.

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