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Sharon Rosenzweig-Lipson

Researcher at Princeton University

Publications -  88
Citations -  4651

Sharon Rosenzweig-Lipson is an academic researcher from Princeton University. The author has contributed to research in topics: Agonist & Receptor. The author has an hindex of 37, co-authored 87 publications receiving 4358 citations. Previous affiliations of Sharon Rosenzweig-Lipson include Pfizer & Harvard University.

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Anxiolytic-like activity of oxytocin in male mice: behavioral and autonomic evidence, therapeutic implications

TL;DR: The results of this study provide specific behavioral and autonomic evidence of anxiolytic-like effects for oxytocin in males and suggest the potential utility of OTR agonism as a therapeutically relevant mechanism of action for novel anxIOlytics in both sexes.
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Innovative Approaches for the Development of Antidepressant Drugs: Current and Future Strategies

TL;DR: The present review addresses the most exciting approaches in the treatment of depression with selective serotonin reuptake inhibitors and reviews the localization, neurochemical and behavioral data that provide the supporting rationale for each of these targets or target combinations.
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Evidence for sustained elevation of IL-6 in the CNS as a key contributor of depressive-like phenotypes.

TL;DR: Elevations in IL-6 may have a pathophysiological role underlying depression and more specifically resistance to current classes of antidepressant medications and modulation of the IL- 6 signaling pathway may have therapeutic potential for treatment-resistant depression.
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Neuropharmacological profile of novel and selective 5-HT6 receptor agonists: WAY-181187 and WAY-208466.

TL;DR: The pharmacological and neurochemical characterization of two novel and selective 5-HT6 receptor agonists reveal a potential therapeutic role for this receptor in the treatment of some types of anxiety-related disorders (eg OCD) and highlight a previously undescribed role for 5- HT6 receptors to modulate basal GABA and stimulated glutamate transmission.
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Differential regulation of central BDNF protein levels by antidepressant and non-antidepressant drug treatments.

TL;DR: The results suggest that diverse pharmacologic and somatic antidepressant treatments, as well as antipsychotics, increase levels of BDNF protein in the frontal cortex, even though they have different mechanisms of action at neurotransmitter systems.