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dc.contributor.authorCreech, R. D.
dc.contributor.authorLi, Qian
dc.contributor.authorCarrasco, Gonzalo A.
dc.contributor.authorVan de Kar, Louis D.
dc.contributor.authorMuma, Nancy A.
dc.date.accessioned2017-02-16T18:50:31Z
dc.date.available2017-02-16T18:50:31Z
dc.date.issued2012-04
dc.identifier.citationCreech, R., Li, Q., Carrasco, G., Van de Kar, L., & Muma, N. (2012). Estradiol induces partial desensitization of serotonin 1A receptor signaling in the paraventricular nucleus of the hypothalamus and alters expression and interaction of RGSZ1and Gαz. Neuropharmacology, 62(5-6), 2040–2049. http://doi.org/10.1016/j.neuropharm.2012.01.001en_US
dc.identifier.urihttp://hdl.handle.net/1808/23188
dc.description.abstractHyperactivity of hypothalamic-pituitary mediated hormone responses, such as to stimulation with a serotonin 1A (5-HT1A) receptor agonist, are a feature of depression which are normalized with clinical improvement during drug therapy. We previously reported that SSRIs induce desensitization of 5-HT1A receptor signaling in the paraventricular nucleus of the hypothalamus (PVN) while estradiol benzoate (EB) produces a more rapid, partial desensitization. In the current study, time-course and dose-response experiments demonstrated that two once daily doses of EB is the minimum needed to induce the desensitization response as indicated by 5-HT1A receptor-stimulated release of oxytocin and that 10 μg/kg/day EB produces the maximal response, a partial desensitization of approximately 40%. The effects of two once daily injections of 10 μg/kg/day EB on Gαz and RGSZ1 proteins were examined as components of the 5-HT1A receptor signaling system, which mediates the release of oxytocin and adrenocorticotropin hormone. RGSZ1 appears to be a major target for EB-mediated responses in the 5-HT1A receptor signaling system. A 55 kD membrane-associate RGSZ1 protein was greatly increased in the PVN and rest of the hypothalamus and moderately increased in the dorsal hippocampus and amygdala after EB treatment as well as after an acute dose of a 5-HT1A receptor agonist. These results suggest that EB is a candidate for adjuvant therapy with SSRIs to hasten the therapeutic response and that RGSZ1 is a major target of EB therapy which could be explored as a target for novel therapeutic approaches for the treatment of depression.en_US
dc.publisherElsevieren_US
dc.rightsThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 3.0 (CC BY-NC-ND 3.0 US), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject5-HT1Aen_US
dc.subjectNeuroendocrineen_US
dc.subjectOxytocinen_US
dc.subjectRegulators of G protein signaling proteinsen_US
dc.subjectEstrogenen_US
dc.subjectDesensitizationen_US
dc.titleEstradiol induces partial desensitization of serotonin 1A receptor signaling in the paraventricular nucleus of the hypothalamus and alters expression and interaction of RGSZ1and Gαzen_US
dc.typeArticleen_US
kusw.kuauthorCreech, RA
kusw.kuauthorLi, Q
kusw.kuauthorCarrasco, GA
kusw.kuauthorVan de Kar, LD
kusw.kuauthorMuma, NA
kusw.kudepartmentPharmacology and Toxicologyen_US
dc.identifier.doi10.1016/j.neuropharm.2012.01.001en_US
kusw.oaversionScholarly/refereed, author accepted manuscripten_US
kusw.oapolicyThis item meets KU Open Access policy criteria.en_US
dc.rights.accessrightsopenAccess


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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 3.0 (CC BY-NC-ND 3.0 US), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
Except where otherwise noted, this item's license is described as: This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 3.0 (CC BY-NC-ND 3.0 US), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.