Neuropeptides, Neurotransmitters, Neurosteroids, and the Onset of Puberty

  title={Neuropeptides, Neurotransmitters, Neurosteroids, and the Onset of Puberty},
  author={Andrea R Genazzani and Francesca Bernardi and Patrizia Monteleone and Stefano Vincenzo Luisi and Michele Luisi},
  journal={Annals of the New York Academy of Sciences},
Abstract: Puberty results from withdrawal of the “gonadostat” mechanisms and from increased gonadotropin sensitivity to GnRH. It has been hypothesized that GnRH release may be modulated by a non‐steroid‐mediated mechanism. Modifications of neuropeptides, neurotransmitters, and neurosteroids may underlie the onset of pubertal processes. Neuropeptides mainly involved in the control of GnRH release are opioids, neuropeptide Y (NPY), galanin, and corticotropin‐releasing factor (CRF), whereas… 

Allopregnanolone levels decrease after gonadotropin-releasing hormone analog stimulation test in girls with central precocious puberty.

The data suggest the prevalent gonadal allopregnanolone production in CPP subjects and the usefulness of its measurement in the diagnosis of CPP.

Leptin ,neuropeptide Y ,β-endorphin ,gonadotropin ,and estradiol levels in girls before menarche

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Changes of Hypothalamic GnRH-I, POMC and NPY mRNA Expression and Serum IGF-I and Leptin Concentrations during Maturation of Shaoxing Ducks (Anas platyrhynchos)

The results indicate that the down-regulation of POMC and NPY genes in hypothalamus coincides with the up- regulation of GnRH-I gene to initiate sexual maturation in ducks and peripheral IGF-I and leptin may relay the peripheral metabolic status to the central system and contribute to the initiation of the reproductive function in ducks.

Pyroglutamylated RFamide peptide 43 stimulates the hypothalamic-pituitary-gonadal axis via gonadotropin-releasing hormone in rats.

Results suggest that icv QRFP43 activates the hypothalamic-pituitary-gonadal axis via GnRH through in vitro stimulated GnRH release from hypothalamic explants from male rats and from GT1-7 cells.

Androgen-sensitive changes in regulation of restraint-induced adrenocorticotropin secretion between early and late puberty in male rats.

It is concluded that during puberty testosterone induces marked changes in regulation of neuropeptides in pathways known to determine autonomic, neuroendocrine, and behavioral responses to chronic stress.

Is neuropeptide Y responsible for constitutional delay of puberty in girls? A preliminary report

The results corroborate the involvement of NPY in sexual maturation and its role in delayed puberty and confirm the role of IGF-I in this phase of puberty.

Review Article Adrenarche in Comparative Perspective

Comparing the timing of adrenal androgen production, brain development and lactation in rats, rhesus macaques and humans suggests that the neuroprotective effects of DHEAS may protect synaptic plasticity in metabolically active parts of the brain starting approximately at the age of 7, promoting prolonged development of the human prefrontal cortex.



β-Endorphin and dynorphin control serum luteinizing hormone level in immature female rats

It is concluded that β-endorphin and dynorphin rather than Met-enkephalin have a role in regulation of LH secretion in immature female rats, and may represent the first data ascribing a specific physiological function to a particular endorphin.

Opioid Control of Gonadotropin Secretion

Among the various neuropeptides which regulate gonadotropin secretion, endogenous opioid peptides (EOP) play an important role. Substantial evidence suggests a possible key function of for these

Mandatory neuropeptide-steroid signaling for the preovulatory luteinizing hormone-releasing hormone discharge.

Examination of various aspects of the complex spatio-temporal patterning of peptidergic signaling that lead to synchronized development of neural events for the preovulatory LHRH discharge on proestrus finds the nature of neurochemical signaling between the two sites remains to be deciphered.

Inhibition of luteinizing hormone release by morphine and endogenous opiates in cultured pituitary cells.

The converse effects of CRF and naltrexone or beta-endorphin antiserum on LH release indicate that intrapituitary opioid peptides could exert a paracrine inhibitory action on the gonadotroph.

Influence of corticotropin-releasing factor on reproductive functions in the rat.

The results indicate that CRF will lower plasma LH levels and can exert this effect in the absence of circulating steroids of either adrenal or gonadal origin and suggest thatCRF exerts deleterious actions on reproductive functions through brain sites of action which, at least under the experimental mental design used, do not appear to directly involve opiate or peripheral catecholaminergic pathways.

Endogenous opioids participate in the regulation of the hypothalamus-pituitary-luteinizing hormone axis and testosterone's negative feedback control of luteinizing hormone.

The results of these studies suggest that endogenous opioids exist in brain tissue which normally inhibit activity in the hypothalamic-pituitary-LH axis and participate in the androgen-dependent feedback control of LH elaboration by this axis.

Evidence for a role for the neurosteroid allopregnanolone in the modulation of reproductive function in female rats.

The present results suggest that hypothalamic allopregnanolone may be involved in the mechanism of ovulation, affecting hormonal and behavioral events.

Galanin stimulates luteinizing hormone-releasing hormone secretion from arcuate nucleus-median eminence fragments in vitro: involvement of an alpha-adrenergic mechanism.

RGAL stimulates LHRH and PGE2 release from arcuate nucleus-median eminence fragments in vitro in a dose-dependent fashion, indicating that rGAL-induced stimulation of L HRH secretion is exerted through alpha-adrenergic receptors and requires PGE1 as an intracellular mediator.

Stimulatory role of substance P on gonadotropin release in ovariectomized rats.

Results indicate that endogenous hypothalamic SP exerts a tonic stimulatory hypothalamic control of basal gonadotropin release in OVX rats.