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Sriparna Ghosal

Researcher at Yale University

Publications -  27
Citations -  2217

Sriparna Ghosal is an academic researcher from Yale University. The author has contributed to research in topics: Chronic stress & Prefrontal cortex. The author has an hindex of 18, co-authored 25 publications receiving 1491 citations. Previous affiliations of Sriparna Ghosal include École Polytechnique Fédérale de Lausanne & University of Cincinnati.

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Regulation of the hypothalamic-pituitary-adrenocortical stress response

TL;DR: Chronic stress-induced activation of the HPA axis takes many forms (chronic basal hypersecretion, sensitized stress responses, and even adrenal exhaustion), with manifestation dependent upon factors such as stressor chronicity, intensity, frequency, and modality.
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Chronic Stress Increases Prefrontal Inhibition: A Mechanism for Stress-Induced Prefrontal Dysfunction

TL;DR: The data suggest that chronic stress increases synaptic inhibition onto prefrontal glutamatergic output neurons, limiting the influence of the prefrontal cortex in control of stress reactivity and behavior.
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Prefrontal Cortex GABAergic Deficits and Circuit Dysfunction in the Pathophysiology and Treatment of Chronic Stress and Depression.

TL;DR: It is suggested that alterations of GABA interneurons and inhibitory neurotransmission play a causal role in the development of stress-related neurobiological illness, and could identify a new line of GABA related therapeutic targets.
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Ketamine accelerates fear extinction via mTORC1 signaling

TL;DR: The hypothesis that ketamine produces long-lasting mTORC1/protein synthesis and activity dependent effects on neuronal circuits that enhance the expression of extinction and could represent a novel approach for the treatment of PTSD is supported.
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Activity-Dependent Brain-Derived Neurotrophic Factor Release Is Required for the Rapid Antidepressant Actions of Scopolamine.

TL;DR: In this paper, the authors found that activity-dependent BDNF release within the medial prefrontal cortex (mPFC) is necessary for the antidepressant actions of scopolamine, and that anti-BDNF antibody infusions into the mPFC prevented the antidepressant-like behavioral effects.