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William E. Cullinan

Researcher at Marquette University

Publications -  48
Citations -  10546

William E. Cullinan is an academic researcher from Marquette University. The author has contributed to research in topics: Hypothalamus & Stria terminalis. The author has an hindex of 36, co-authored 48 publications receiving 10035 citations. Previous affiliations of William E. Cullinan include College of Health Sciences, Bahrain & University of Virginia.

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Neurocircuitry of stress: central control of the hypothalamo–pituitary–adrenocortical axis

TL;DR: The functional and neuroanatomical data obtained suggest that disease processes involving inappropriate stress control involve dysfunction of processive stress pathways.
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Central mechanisms of stress integration: hierarchical circuitry controlling hypothalamo-pituitary-adrenocortical responsiveness.

TL;DR: The principle extrinsic and intrinsic mechanisms responsible for regulating stress-responsive CRH neurons of the hypothalamic paraventricular nucleus, which summate excitatory and inhibitory inputs into a net secretory signal at the pituitary gland, are reviewed.
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Pattern and time course of immediate early gene expression in rat brain following acute stress.

TL;DR: The present results reveal a widespread pattern of neuronal activation in response to acute swim or restraint stress that may aid in the identification of stress-specific neural circuits and are likely to have important implications for the understanding of neuronal regulation of the stress response.
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Ventral subicular interaction with the hypothalamic paraventricular nucleus : evidence for a relay in the bed nucleus of the stria terminalis

TL;DR: The axonal projections of the ventral subiculum to the bed nucleus of the stria terminalis (BST) were examined in the rat with the anterograde neuronal tracer Phaseolus vulgaris‐ leucoagglutinin (PHA‐L) and provided light microscopic evidence for subicular input to PVN‐projecting cells located within the BST.
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Endocannabinoid Signaling Negatively Modulates Stress-Induced Activation of the Hypothalamic-Pituitary-Adrenal Axis

TL;DR: Data indicate that e CB signaling negatively modulates HPA axis function in a context-dependent manner and suggest that pharmacological augmentation of eCB signaling could serve as a novel approach to the treatment of anxiety-related disorders.