Estradiol and progesterone-induced lordosis behavior is modulated by both the Kisspeptin receptor and melanin-concentrating hormone in estradiol benzoate-primed rats
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
36115135
DOI
10.1016/j.yhbeh.2022.105257
PII: S0018-506X(22)00151-9
Knihovny.cz E-resources
- Keywords
- Estradiol, Kisspeptin, Lordosis, Melanin-concentrating hormone, Progesterone,
- MeSH
- Estradiol pharmacology MeSH
- Gonadotropin-Releasing Hormone pharmacology MeSH
- Kisspeptins pharmacology MeSH
- Rats MeSH
- Lordosis * chemically induced MeSH
- Ovariectomy MeSH
- Progesterone * pharmacology MeSH
- Sexual Behavior, Animal physiology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- estradiol 3-benzoate MeSH Browser
- Estradiol MeSH
- Gonadotropin-Releasing Hormone MeSH
- Kisspeptins MeSH
- melanin-concentrating hormone MeSH Browser
- Progesterone * MeSH
Intracerebroventricular (ICV) administration of estradiol benzoate (E2B) and progesterone (P) induces intense lordosis behavior in ovariectomized rats primed peripherally with E2B. The present study tested the hypothesis that the Kisspeptin (Kiss) and melanin-concentrating hormone (MCH) pathways regulate female sexual behavior induced by these steroid hormones. In Experiment 1, we tested the relevance of the Kiss pathway by ICV infusion of its inhibitor, kiss-234, before administration of E2B or P in estrogen-primed rats. Lordosis induced by E2B alone or with the addition of P was reduced significantly at 30, 120, and 240 min. In Experiment 2, ICV infusion of MCH 30 min before E2B or P significantly reduced lordosis in rats primed with E2B alone. These data support the hypothesis that the Kiss and MCH pathways, which can release or modulate gonadotropin-releasing hormone (GnRH), are involved in E2B- and P-induced lordosis.
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