GnRH is a tropic peptide hormone synthesized and released from GnRH neurons within the hypothalamus.
Gonadotropin-releasing hormone (GnRH) is a releasing hormone responsible for the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary.
GnRH is a peptide hormone synthesized and released from GnRH neurons within the hypothalamus.
The GnRH neurons originate in the nose and migrate into the brain.
The GnRH neurons on the brain are scattered throughout the medial septum and hypothalamus and connected by very long >1-millimeter-long dendrites.
The GnRH neurons bundle together so they receive shared synaptic input, a process that allows them to synchronize their GnRH release.
The GnRH neurons are regulated by different afferent neurons, and use several neurotransmitters, including norepinephrine, GABA, glutamate.
GnRH constitutes the initial step in the hypothalamic-pituitary-gonadal axis.
Chromosome 8 location.
The gene, GNRH1, for the GnRH precursor is located on chromosome 8.
GNRH1, the GnRH precursor is located on chromosome 8.
It is synthesized from an 89-amino acid preprohormone in the preoptic anterior hypothalamus.
It is the target of regulatory mechanisms of the hypothalamic-pituitary-gonadal axis, such as being inhibited by increased estrogen levels in the body.
GnRH is secreted in the hypophysial portal bloodstream at the median eminence.
The portal bloodstream carries GnRH to the pituitary gland, which contains the gonadotrope cells, where GnRH activates its own receptor, gonadotropin-releasing hormone receptor (GnRHR)
Gonadotropin-releasing hormone receptor (GnRHR) is a seven transmembrane G-protein-coupled receptor that stimulates that results in the activation of proteins involved in the synthesis and secretion of the gonadotropins LH and FSH.
GnRH is degraded by proteolysis within a few minutes.
During childhood GnRH activity is very low and is activated in puberty or adolescence.
Pulse activity is critical for successful reproductive function as controlled by feedback loops.
With pregnancy GnRH activity is not required.
The normal pulsatile activity can be disrupted by any hypothalamic-pituitary disease.
GnRH pulsatile activity can be disrupted by hypothalamic-pituitary disease, hypothalamic suppression or organic lesions of trauma, or tumor.
Elevation in prolactin levels decrease GnRH activity.
Hyperinsulinemia increases pulse activity leading to disorderly LH and FSH activity, as seen in polycystic ovary syndrome.
GnRH formation is absent in Kallmann syndrome.
GnRH in the pituitary stimulates the synthesis and secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH).
The. synthesis of FSH. LH are controlled by the size and frequency of GnRH pulses, as well as by feedback from androgens and estrogens.
Low-frequency GnRH pulses are required for FSH release.
High-frequency GnRH pulses stimulate LH pulses.
In males, GnRH is secreted in pulses at a constant frequency.
In females, the frequency of the pulses varies during the menstrual cycle, and there is a large surge of GnRH just before ovulation.
GnRH1, controls a complex process of follicular growth, ovulation, and corpus luteum maintenance in the female, and spermatogenesis in the male.
It is considered a neurohormone, produced in a specific neural cell and released at its neural terminal.
The preoptic area of the hypothalamus, contains most of the GnRH-secreting neurons.
GnRH neurons originate in the nose and migrate into the brain.
In this migration they are scattered throughout the medial septum and hypothalamus and connected by very long dendrites.
The dendrites bundle to synchronize their GnRH release.
The GnRH neurons are regulated by different afferent neurons, using several different transmitters.
These transmitters include: norepinephrine, GABA, glutamate.
Dopamine stimulates LH release through GnRH in estrogen-progesterone-primed females.
Dopamine may inhibit LH release in ovariectomized females.
GnRH is found in organs outside of the hypothalamus and pituitary:
placenta and in the gonads,breast, ovary, prostate, and endometrium.
Synthetic analogs have replaced the natural hormone in clinical use.
Its analogue leuprorelin is used to to treat breast cancer, endometriosis, prostate cancer, and precocious puberty.
Modifications of structure of GnRH to increase half life have led to GnRH1 analog medications that either stimulate (GnRH1 agonists) or suppress (GnRH antagonists) the gonadotropins.
Its analogue leuprorelin is used for continuous infusion, to treat breast cancer, endometriosis, prostate cancer, and precocious puberty.
GnRH agonists protect the ovaries during chemotherapy, in terms of menstruation recovery, ovarian failure and ovulation.
Increased levels of GnRH facilitate sexual displays and behavior in females.
An elevation of GnRH raises male’s testosterone capacity beyond its natural testosterone level.
A impaired GnRH system has adverse effects on reproductive physiology and maternal behavior.
Effective in protecting the ovaries during chemotherapy, in terms of menstruation recovery or maintenance, premature ovarian failure and ovulation.