Participation of kisspeptin, progesterone, and GnRH receptors on lordosis behavior induced by kisspeptin
Language English Country United States Media print-electronic
Document type Journal Article
PubMed
38851441
DOI
10.1016/j.physbeh.2024.114609
PII: S0031-9384(24)00154-9
Knihovny.cz E-resources
- Keywords
- Antide, Kiss-234, Kisspeptin, Lordosis behavior, RU486,
- MeSH
- Hormone Antagonists pharmacology MeSH
- Estradiol * pharmacology analogs & derivatives MeSH
- Kisspeptins * pharmacology metabolism MeSH
- Rats MeSH
- Mifepristone pharmacology MeSH
- Ovariectomy MeSH
- Posture physiology MeSH
- Rats, Wistar MeSH
- Progesterone pharmacology MeSH
- Receptors, Kisspeptin-1 metabolism MeSH
- Receptors, LHRH * antagonists & inhibitors metabolism MeSH
- Receptors, Progesterone * metabolism drug effects antagonists & inhibitors MeSH
- Sexual Behavior, Animal * drug effects physiology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Hormone Antagonists MeSH
- estradiol 3-benzoate MeSH Browser
- Estradiol * MeSH
- Kisspeptins * MeSH
- Mifepristone MeSH
- Progesterone MeSH
- Receptors, Kisspeptin-1 MeSH
- Receptors, LHRH * MeSH
- Receptors, Progesterone * MeSH
The neuropeptide kisspeptin (Kiss) is crucial in regulating the hypothalamic-pituitary-gonadal axis. It is produced by two main groups of neurons in the hypothalamus: the rostral periventricular region around the third ventricle and the arcuate nucleus. Kiss is the peptide product of the KiSS-1 gene and serves as the endogenous agonist for the GPR54 receptor. The Kiss/GPR54 system functions as a critical regulator of the reproductive system. Thus, we examined the effect of intracerebroventricular administration of 3 μg of Kiss to the right lateral ventricle of ovariectomized rats primed with a dose of 5 μg subcutaneous (sc) of estradiol benzoate (EB). Kiss treatment increased the lordosis quotient at all times tested. However, the lordosis reflex score was comparatively lower yet still significant compared to the control group. To investigate receptor specificity and downstream mechanisms on lordosis, we infused 10 μg of GPR54 receptor antagonist, Kiss-234, 5 μg of the progestin receptor antagonist, RU486, or 3 μg of antide, a gonadotropin-releasing hormone-1 (GnRH-1) receptor antagonist, to the right lateral ventricle 30 min before an infusion of 3 μg of Kiss. Results demonstrated a significant reduction in the facilitation of lordosis behavior by Kiss at 60 and 120 min when Kiss-234, RU486, or antide were administered. These findings suggest that Kiss stimulates lordosis expression by activating GPR54 receptors on GnRH neurons and that Kiss/GPR54 system is an essential intermediary by which progesterone activates GnRH.
Doctorado en Ciencias Biológicas Universidad Autónoma de Tlaxcala Tlaxcala México
Instituto de Investigaciones Cerebrales Universidad Veracruzana Veracruz México
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