The Relationship between Drug-Induced Neurogenesis and Pain Behavior in Mice.

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2008
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Haverford College. Department of Psychology
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Thesis
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Award
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eng
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Open Access
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Abstract
This experiment aims to study the relationship between neurogenesis and pain by inducing varying amounts of neurogenesis in mice using a pharmacological manipulation and to evaluate the subsequent pain behavior. A muscarinic ACh receptor agonist, galantamine, was used to increase neurogenesis and a nicotinic ACh receptor agonist, nicotine, was intended to decrease neurogenesis. Injections were administered daily for two weeks to two different drug condition groups and a saline control group, with N = 10 male mice and N = 10 female mice in each group. It was hypothesized that rates of neurogenesis (measured by the number of BrdU positive cells/μm³) would vary across condition, with animals receiving nicotine expressing the lowest rate of neurogenesis and animals receiving galantamine expressing the highest rate of neurogenesis. It was additionally hypothesized that pain behavior on the formalin test would vary across condition in the same direction as neurogenesis. Although the directionality was not as hypothesized, there was a significant effect of the drug conditions in the late phase of pain, with saline-treated animals expressing the lowest amount of pain behavior and galantamine-treated animals expressing the highest amount of pain behavior on average. There was also a significant main effect of condition on our measure of neurogenesis, and the directionality of the effect was the same as that of pain behavior. Our results provide evidence for a relationship between drug-induced neurogenesis and pain behavior in mice, which holds implications for further neurogenesis research.
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