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Kathryn M. Buller

Researcher at University of Queensland

Publications -  62
Citations -  3664

Kathryn M. Buller is an academic researcher from University of Queensland. The author has contributed to research in topics: Stria terminalis & Hypothalamus. The author has an hindex of 30, co-authored 62 publications receiving 3436 citations. Previous affiliations of Kathryn M. Buller include University of Otago & Royal Brisbane and Women's Hospital.

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Stressor categorization: acute physical and psychological stressors elicit distinctive recruitment patterns in the amygdala and in medullary noradrenergic cell groups.

TL;DR: The present data support the suggestion that the brain recognizes at least two major categories of stressor, which the authors have referred to as ‘physical’ and ‘psychological’.
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Chronic stress alters the density and morphology of microglia in a subset of stress-responsive brain regions

TL;DR: It is demonstrated that chronic stress selectively increases the number of microglia in certain stress-sensitive brain regions, and also causes a marked transition of microGlia from a ramified-resting state to a non-Resting state, consistent with the view that microglial activation could play an important role in controlling and/or adapting to stress.
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Neuroendocrine responses to an emotional stressor: evidence for involvement of the medial but not the central amygdala.

TL;DR: Findings provide the first direct evidence that it is the medial rather than the central amygdala that is critical to hypothalamic neuroendocrine cell responses during an emotional response, and also provides the first evidence that the amygdala governs oxytocin as well as HPA axis responses to an emotional stressor.
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Medial prefrontal cortex control of the paraventricular hypothalamic nucleus response to psychological stress: possible role of the bed nucleus of the stria terminalis.

TL;DR: A set of connections is suggested whereby a direct PVN projection from the ipsilateral vBNST is involved in the mpPVN response to air puff and this may, in turn, be modulated by an indirect projections from the mPFC to the BNST.
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Therapeutic activity of C5a receptor antagonists in a rat model of neurodegeneration

TL;DR: It is demonstrated for the first time that complement activation in the brain, particularly C5a, is a key event in the pathogenesis of this disease model, and suggest a future role for inhibitors of C 5a in the treatment of neurodegenerative diseases.