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Endocrinology
August 2021
Harvard Medical School, Boston, MA 02115, USA.
The alternation of the stimulatory action of the tachykinin neurokinin B (NKB) and the inhibitory action of dynorphin within arcuate (ARH) Kiss1 neurons has been proposed as the mechanism behind the generation of gonadotropin-releasing hormone (GnRH) pulses through the pulsatile release of kisspeptin. However, we have recently documented that GnRH pulses still exist in gonadectomized mice in the absence of tachykinin signaling. Here, we document an increase in basal frequency and amplitude of luteinizing hormone (LH) pulses in intact male mice deficient in substance P, neurokinin A (NKA) signaling (Tac1KO), and NKB signaling (Tac2KO and Tacr3KO).
View Article and Find Full Text PDFTemperature (Austin)
November 2017
Departments of Pathology (S.J.K-H., E.M.B., J.R.M. and N.E.R.), Cellular and Molecular Medicine (N.E.R.), Neurology (N.E.R.) and the Evelyn F. McKnight Brain Institute (N.E.R.) University of Arizona College of Medicine, Tucson, AZ, USA.
Hot flushes are due to estrogen withdrawal and characterized by the episodic activation of heat dissipation effectors. Recent studies (in humans and rats) have implicated neurokinin 3 (NK) receptor signaling in the genesis of hot flushes. Although transgenic mice are increasingly used for biomedical research, there is limited information on how 17β-estradiol and NK receptor signaling alters thermoregulation in the mouse.
View Article and Find Full Text PDFEndocrinology
October 2017
Department of Obstetrics & Gynecology, University of Washington, Seattle, Washington 98195.
Vasomotor symptoms (VMS; or hot flashes) plague millions of reproductive-aged men and women who have natural or iatrogenic loss of sex steroid production. Many affected individuals are left without treatment options because of contraindications to hormone replacement therapy and the lack of equally effective nonhormonal alternatives. Moreover, development of safer, more effective therapies has been stymied by the lack of an animal model that recapitulates the hot-flash phenomenon and enables direct testing of hypotheses regarding the pathophysiology underlying hot flashes.
View Article and Find Full Text PDFEndocrinology
July 2017
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115.
The tachykinins substance P (SP) and neurokinin A (Tac1) have emerged as novel regulators of kisspeptin/GnRH release. Recently, we documented that SP modulates reproductive function in the female mouse. Here, we extended this characterization to the male mouse.
View Article and Find Full Text PDFBehav Brain Res
April 2016
Department of Pharmacology, Federal University of Santa Catarina, Florianópolis, SC 88049-900, Brazil.
Introduction: Substance P (SP) is a neuropeptide widely expressed throughout the fear-processing pathways of the brain. SP is cleaved by several proteolytic enzymes in amino (N-) and carboxy (C-) terminal sequences, which can have biological activities per se. We have previously shown that the anxiogenic-like effects elicited by SP6-11(C-terminal), a specific metabolite of SP, are mediated via NK1 and NK2 receptors.
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