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Endocrine Functions of Brain Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Both sets of neurons project to GnRH cell bodies, which contain the kisspeptin receptor Kiss1R. Kisspeptin neurons in the arcuate nucleus also co-express neurokinin B and the endogenous opioid peptide, dynorphin, and are named kisspeptin/neurokinin B/dynorphin (KNDy) neurons. The kisspeptin neurons in the rostral periventricular area play an essential role in enabling ovulation in rodents by activating the GnRH neurons, while those in the arcuate nucleus are involved in the regulation of pulsatile GnRH release and also mediate the negative feedback of the sex steroids on the HPG axis given that GnRH neurons themselves do not express receptors for gonadal steroids (Figure 4.12).
Receptors for Neuropeptides (Neurokinins): Functional Studies
Published in Edwin E. Daniel, Neuropeptide Function in the Gastrointestinal Tract, 2019
D. Regoli, S. Dion, G. Drapeau
These various effects are brought about by the activation of multiple receptors whose existence was suggested from early findings by the Erspamer group.13 In 1982, a comparison of data obtained in different isolated organs (intestinal, extraintestinal) brought Lee et al.14 to suggest the existence of two different receptor types named SP-P and SP-E. Further progress was made when the other two mammalian neurokinins (neurokinin A and neurokinin B) were identified15 and when it was shown that each natural neurokinin may have its own receptor.16 Shortly after, three receptor types were identified with biological17 and biochemical assays.18 The three-receptor hypothesis was further confirmed and definitely demonstrated by the use of selective agonists.19,20 The three receptors have been named NK-1, NK-2, and NK-3 to indicate the receptors for substance P (SP), neurokinin A (NKA), and neurokinin B (NKB), respectively. 21
Problems with puberty and its onset
Published in David J Cahill, Practical Patient Management in Reproductive Medicine, 2019
While the trigger for the onset of puberty is still unclear, there is increasing knowledge about the peptides that control the secretion of GnRH by the arcuate nucleus (12). A group of neurones, the anteroventral periventricular nucleus – sited close to the lateral walls of the third ventricle in the preoptic area – and neurones in the arcuate nucleus release kisspeptin, a neuropeptide hormone, so named because it was first identified in Hershey, Pennsylvania, USA, the home of Hershey's Kisses (14). Receptors for kisspeptin (KISS1R), found in the anteroventral periventricular nucleus, seem to be as important as the hormone itself. Absence of the gene for the receptor has been linked with idiopathic hypogonadotrophic hypogonadism (15). Gamma-aminobutyric acid (GABA – suppressive) and glutamate (stimulatory) are also active at the anteroventral periventricular nucleus level, while at the arcuate nucleus, kisspeptin neurones also secrete neurokinin B and dynorphin A (Figure 1.4). Before puberty starts, dynorphin A has a dominant inhibitory influence. As puberty starts, neurokinin B increases in its stimulatory drive overcoming dynorphin A, allowing kisspeptin to become active and stimulatory as well (12). From this, it seems reasonable to speculate that whatever increases neurokinin B is the responsible factor for the initiation of the GnRH pulses.
Managing vasomotor symptoms effectively without hormones
Published in Climacteric, 2020
C. A. McCormick, A. Brennan, M. Hickey
Menopause is a normal reproductive stage marking the end of reproductive life. Characteristic changes in ovarian sex steroid production lead to changes in menstrual bleeding patterns and commonly induce symptoms that may affect quality of life, work attendance and productivity, and intimate relationships1. Vasomotor symptoms (VMS; hot flushes and/or night sweats) affect around 80% of women over the menopause transition, are the main reason for seeking medical advice, and are the leading patient priority for treatment2. Currently, VMS are thought to result from upregulation of neurokinin B secondary to estrogen deficiency3. Neurokinin B interacts with the autonomic thermoregulatory pathway. Directly targeting this pathway is an area of growing clinical interest in non-hormonal treatments for VMS4.
Temperature regulation in women: Effects of the menstrual cycle
Published in Temperature, 2020
Fiona C. Baker, Felicia Siboza, Andrea Fuller
Over its duration of 25 to 35 days, the menstrual cycle is characterized by cyclical changes in hormones across the hypothalamic-pituitary-ovarian system (Figure 1), which are regulated by feedback mechanisms. Estradiol (the most potent estrogen) is the main secretory product of the ovarian follicle during the early follicular phase of the cycle and, together with inhibin, is primarily responsible for inducing a negative feedback regulation on the release of the gonadotrophins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), from the pituitary [41,42]. In the late follicular phase, as ovarian follicles develop and mature, estradiol is secreted in large amounts; when the estradiol concentration has exceeded a certain threshold for a certain amount of time (>200 pg.ml−1 for ~48 h [43]), it switches to exerting positive feedback on the hypothalamic-pituitary system, sensitizing the pituitary to the hypothalamic peptide gonadotrophin-releasing hormone (GnRH), leading to the mid-cycle LH surge [41,42]. Progesterone, on the other hand, which rises early in the luteal phase, inhibits pulsatile GnRH and, consequently, LH release; it also prevents the positive feedback effect of elevated estrogen on GnRH and LH [44]. Kisspeptin and neurokinin B, neuropeptides secreted by the ventral hypothalamus, play a key role in regulating GnRH and subsequent gonadotropin secretion [45].
Managing vasomotor symptoms in women after cancer
Published in Climacteric, 2019
Data are emerging about the effectiveness of neurokinin B antagonists in the treatment of menopausal hot flashes. While data remain limited, these neurokinin antagonists appear to have a remarkably fast onset of action, within the first 1 or 2 days of administration, and have a significant effect on both daytime flashes and night sleep disturbance. If safety and long-term efficacy are confirmed, these new agents will be an important advance in non-hormone therapy for hot flashes. The neurokinin B pathway is involved in physiological regulation of the control of gonadotropin-releasing hormone secretion in men and women, and is a key mediator of hot flashes. Neurokinin B antagonists have shown remarkable rapid efficacy in reducing hot flash frequency, for both daytime and nighttime hot flashes60.