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Rong Zhang

Researcher at University of Cincinnati

Publications -  8
Citations -  492

Rong Zhang is an academic researcher from University of Cincinnati. The author has contributed to research in topics: Chronic stress & Corticosterone. The author has an hindex of 7, co-authored 7 publications receiving 436 citations.

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Stress vulnerability during adolescent development in rats.

TL;DR: Testing the hypothesis that adolescent development is a stage of enhanced vulnerability to chronic stress shows that adolescent animals were protected from the effect of chronic stress on depression-like behavior while late adolescents animals were more susceptible to the somatic, HPA axis, and neuropeptide effects of Chronic stress.
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Stress activation of IL-6 neurons in the hypothalamus

TL;DR: IL-6 neurons of the HNS are a recruited component of the response to psychological stress, and data indicate that noninflammatory stressors selectively activate IL-6 magnocellular neurons, upregulate IL-8 gene expression in the PVN and SON, and increase plasma IL- 6.
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Distribution of glucagon-like peptide-1 immunoreactivity in the hypothalamic paraventricular and supraoptic nuclei

TL;DR: Overall, the data indicate that the central GLP-1 system preferentially targets neurons in hypophysiotrophic zones of the PVN, consistent with excitatory actions of GLp-1 on adrenocorticotropin release.
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Neuroendocrine Function After Hypothalamic Depletion of Glucocorticoid Receptors in Male and Female Mice

TL;DR: Results reveal pronounced sex differences in the PVN GR dependence of acute stress feedback regulation of HPA axis function and indicate that glucocorticoid control of H PA axis responses after chronic stress operates via a PVN-independent mechanism.
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Glucocorticoid regulation of preproglucagon transcription and RNA stability during stress

TL;DR: It is suggested that glucocorticoids deplete the pool of transcribed PPG RNA and concurrently stimulate PPG gene transcription, with the latter allowing a mechanism for replenishment of PPG mRNA after stress cessation, resulting in a transient reduction in the capacity for neuropeptidergic excitation of stress responses.