The researchers found a regulatory medium between stress and infertility

It is well known that long-term or excessive stress perception has some negative effects on fertility in humans and animals, acute stress responses can lead to reproductive delays, and chronic stress can lead to long-term infertility.
reproductive function is regulated by the hypothyroidist-pituitary gland (HPG) hormone axis, and hypothyroid glandular hormone release hormone (GnRH) neurons regulate pituitary secretion of progesterone (LH) and follicle stimulator (FSH) to maintain optimal reproductive function.
stress-induced reproductive dysfunction is usually associated with increased activation of the hypothyroid-pituitary-adrenal (HPA) axis and the continued release of glucoticoids.
how activation of the HPA axis and elevated glucosal hormone levels affect GnRH neurons and inhibit LH and FSH secretion is not yet known.
Recently, researchers from the University of Otago in New Zealand published a study in journal of Neuroscience entitled RFamide-related peptide neurons and stress responses, which found that RFRP neurons are a key regulator between stress and infertility and may become active under stress conditions, thereby inhibiting LH secretion and affecting the reproductive system.
RFFamide-related peptide 3 (RFRP-3) is a peptide secreted by RFRP neurons that inhibits GnRH activity.
study found that acute binding stress inhibited LH secretion in male mice and increased the activity of RFRP neurons.
about half of RFRP neurons can express glucoticoids, and adrenal excision prevents the effects of binding stress on the expression of the Rfrp gene.
suggests that adrenal glucoticoids activate RFRP neurons under stress.
this leads to speculation that RFRP neurons may be the media for stress-induced HPG axis suppression? To test this hypothesis, the researchers first constructed and validated a novel RFRP-Cre mouse line and then combined it with Cre-dependent neuron ablation and DREDD technology to selectively ablation, stimulate and inhibit RFRP neurons to study their physiological role in fertility and stress response regulation.
the production and validation of the new RFRP-Cre mouse line by researchers using chlorine-nitrogen-N-oxide (CNO) to acutely activate RFRP neurons in test mice, and found that glucoticoid release increased about fourfold.
activation of RFRP neurons caused reproductive damage in mice, leading to delayed puberty in male mice and longer cycles in female mice.
RFRP-hM3Dq neuron activation delayed male puberty episodes and prolonged female cycle length by using diphtheria toxin to ablation of RFRP neurons in mice, it was found that it had no effect on glucoticoid concentration and mouse cycle.
tested the LH concentration and pulse after the baseline period, 30 minutes of binding stress and stress period, and found that the female mice with RFRP ablation showed no pressure-induced LH concentration reduction and pulse suppression compared to the pressure-induced LH concentration and pulse suppression in the control group mice.
RFRP neuron ablation prevents acute stress-induced LH inhibition of chronic glucosticoid therapy, which inhibits LH pulses in female mice, and the researchers found that female mice that were silent compared to the control group did not exhibit binding stress-induced LH secretion and pulse suppression when treated with chronic glucoticoids.
male mice with silencing RFRP neurons showed significant inhibition and pulse frequencies at LH concentrations similar to those induced by corticosteroids in the control group.
also suggests that the secretion of pulsed reproductive hormones by the rheumine RFRP neurons as a medium to suppress stress-induced is unique to females (females).
M. Anderson, who co-authored the study, said: "For women struggling with infertility, the use of drugs that block the action of RFRP neurons may be a novel treatment.
and as far as we know about these neurons, the drug won't have any side effects.
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