R
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
Matia B. Solomon,Matthew C. Loftspring,Annette D. de Kloet,Sriparna Ghosal,Ryan Jankord,Jonathan N. Flak,Aynara C. Wulsin,Eric G. Krause,Rong Zhang,Taylor Rice,Jessica M. McKlveen,Brent Myers,Jeffrey G. Tasker,James P. Herman +13 more
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.