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Nicole D. Powell

Researcher at Ohio State University

Publications -  33
Citations -  3370

Nicole D. Powell is an academic researcher from Ohio State University. The author has contributed to research in topics: Experimental autoimmune encephalomyelitis & Immune system. The author has an hindex of 23, co-authored 33 publications receiving 2876 citations. Previous affiliations of Nicole D. Powell include The Ohio State University Wexner Medical Center.

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β-Adrenergic Receptor Antagonism Prevents Anxiety-like Behavior and Microglial Reactivity Induced by Repeated Social Defeat

TL;DR: It is shown that repeated social defeat in mice increased c-Fos staining in brain regions associated with fear and threat appraisal and promoted anxiety-like behavior in a β-adrenergic receptor-dependent manner.
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Social stress up-regulates inflammatory gene expression in the leukocyte transcriptome via β-adrenergic induction of myelopoiesis

TL;DR: The results suggest that sympathetic nervous system-induced up-regulation of myelopoiesis mediates the proinflammatory component of the leukocyte CTRA dynamic and may contribute to the increased risk of inflammation-related disease associated with adverse social conditions.
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Stress-induced recruitment of bone marrow-derived monocytes to the brain promotes anxiety-like behavior.

TL;DR: It is shown that RSD-induced anxiety-like behavior corresponded with an exposure-dependent increase in circulating monocytes and brain macrophages and monocyte recruitment to the brain in response to social stress represents a novel cellular mechanism that contributes to the development of anxiety.
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Peripheral innate immune challenge exaggerated microglia activation, increased the number of inflammatory CNS macrophages, and prolonged social withdrawal in socially defeated mice.

TL;DR: Findings demonstrate that repeated social defeat enhanced the neuroinflammatory response and caused prolonged sickness following innate immune challenge.
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Re-establishment of anxiety in stress-sensitized mice is caused by monocyte trafficking from the spleen to the brain.

TL;DR: The findings show that neuroinflammatory mechanisms promote mood disturbances following stress-sensitization and outline novel neuroimmune interactions that underlie recurring anxiety disorders such as posttraumatic stress disorder.