Kisspeptin regulates tuberoinfundibular dopaminergic neurones and prolactin secretion in an oestradiol-dependent manner in male and female rats.
Ribeiro. A B AB; Leite. C M CM; Kalil. B B; Franci. C R CR; Anselmo-Franci. J A JA; Szawka. R E RE
Key Findings
- Kisspeptin‑10 raises blood prolactin levels when estrogen is present, by reducing dopamine activity in the brain’s tuberoinfundibular pathway.
- The prolactin‑boosting effect is seen in both sexes, but requires estrogen (or testosterone that can be converted to estrogen) – it does not occur in hormone‑deficient (ovariectomised or castrated) rats without estrogen replacement.
- LH release in response to kisspeptin‑10 does not depend on estrogen, indicating separate pathways for prolactin and LH regulation.
Practical Outcomes
- For biohackers, this research suggests that kisspeptin could be used to modulate prolactin, but only in the context of adequate estrogen levels. Because the experiments used direct brain injections in rats, there’s no ready‑to‑use dosing protocol for humans. The finding mainly adds to the understanding of how hormones interact, which might inform future strategies for managing prolactin‑related issues such as recovery, sleep, or metabolic effects, but it isn’t immediately actionable.
Summary
In rats, the peptide kisspeptin-10 boosts the hormone prolactin by turning down dopamine signals that normally keep prolactin low. This effect only happens when estrogen (or a similar hormone) is present, and it works in both male and female animals. The study shows that kisspeptin’s impact on prolactin is separate from its well‑known role in controlling reproductive hormones like LH.
Abstract
Prolactin (PRL) secretion is inhibited by hypothalamic dopamine. Kisspeptin controls luteinising hormone (LH) secretion and is also involved in PRL regulation. We further investigated the effect of kisspeptin-10 (Kp-10) on the activity of tuberoinfundibular dopaminergic (TIDA) neurones and the role of oestradiol (E2 ) in this mechanism. Female and male rats were injected with i.c.v. Kp-10 and evaluated for PRL release and the activity of dopamine terminals in the median eminence (ME) and neurointermediate lobe of the pituitary (NIL). Kp-10 at the doses of 0.6 and 3 nmol increased plasma PRL and decreased 4-dihydroxyphenylacetic acid (DOPAC) levels in the ME and NIL of ovariectomised (OVX), E2 -treated rats but had no effect in OVX. In gonad-intact males, 3 nmol Kp-10 increased PRL secretion and decreased DOPAC levels in the ME but not in the NIL. Castrated males treated with either testosterone or E2 also displayed increased PRL secretion and reduced ME DOPAC in response to Kp-10, whereas castrated rats receiving oil or dihydrotestosterone were unresponsive. By contrast, the LH response to Kp-10 was not E2 -dependent in either females or males. Additionally, immunohistochemical double-labelling demonstrated that TIDA neurones of male rats contain oestrogen receptor (ER)-α, with a higher proportion of neurones expressing ERα than in dioestrous females. The dopaminergic neurones of periventricular hypothalamic nucleus displayed much lower ERα expression. Thus, TIDA neurones express ERα in male and female rats, and kisspeptin increases PRL secretion through inhibition of TIDA neurones in an E2 -dependent manner in both sexes. These findings provide new evidence about the role of kisspeptin in the regulation of dopamine and PRL.
Study Information
pubmed
2015
2015-02-01T00:00:00.000Z
10.1111/jne.12242
44
70