Differential effects of the N-methyl-d-aspartate and non-N-methyl-d-aspartate receptors of the excitatory amino acids system on LH and FSH secretion. Its effects on the hypothalamic luteinizing hormone releasing hormone during maturation in male rats

Carbone, Silvia; Szwarcfarb, Berta; Rondina, Dora; Feleder, Carlos; Moguilevsky, Jaime A.

doi:10.1016/0006-8993(95)01216-8

Cited by 28 publications

(16 citation statements)

References 29 publications

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“…In terestingly. hypothalamic fragments of 30-day-old peripu bertal animals were significantly more sensitive to kainate of NMDA than 16-day-old animals [31]. These data sug gest that a postnatal maturation process of the brain-pituitary-gonadal axis occurs toward the initiation of puberty which includes a heightened responsiveness to glutamate.…”

Section: Discussionsupporting

confidence: 51%

Expression of Glutamate Receptor Subunit mRNAs in Gonadotropin-Releasing Hormone Neurons during the Sexual Maturation of the Female Rat

Eyigor

Jennes²

1997

Neuroendocrinology

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Excitatory amino acids, particularly glutamate, are thought to be important for the maturation of the brain-pituitary-gonadal axis and the induction of puberty in the rat. We have previously shown that, in the female rat, GnRH neurons preferentially express the KA2 and NMDAR2A receptor subunit mRNAs, but not AMPA or NMDAR1 mRNA. The aim of the present study was to determine whether the onset or rate of KA2 and NMDAR2A receptor expression in GnRH neurons is correlated with the onset of puberty. Dual in situ hybridization using digoxigenin-labeled GnRH cRNA probes and ³⁵S-labeled glutamate receptor subunit probes, followed by autoradiography and image analysis were used to measure the KA2 or NMDAR2A mRNA content in GnRH neurons in 20- to 50-day-old female rats which were sacrificed at 08.00 or 17.00 h. The results show that: (a) the KA2 mRNA content of GnRH neurons and the number of GnRH neurons expressing KA2 mRNA increase progressively in the morning hours between postnatal days 20 and 40; (b) the diurnal pattern of KA2 mRNA levels in GnRH neurons changes between days 40 and 50 from high KA2 levels in the morning hours before day 40 to high KA2 mRNA levels in the afternoon in 45- and 50-day-old animals; (c) while the high levels of KA2 mRNA in GnRH neurons in the morning hours of 20-to 40-day-old animals are paralleled by an overall increase in KA2 expression in the preoptic area, the rise in KA2 mRNA in GnRH neurons in the afternoon of 45- and 50-day-old animals appears to be specific for the GnRH neurons, and (d) no significant differences were detected for the NMDAR2A mRNA content in GnRH neurons among the different age groups and the morning and afternoon values. Since the gradual increase in the KA2 mRNA content in GnRH neurons of animals reaching puberty as well as the reversal of diurnal rhythmicity in KA2 receptor mRNA content of GnRH neurons coincide with the times of vaginal opening and first ovulation, it is suggested that glutamate, acting through KA2 receptors directly on GnRH neurons is, at least in part, an important factor in the excitatory regulation of the postnatal sexual development of the female rat. In contrast, expression of the NMDA-preferring receptor, NMDAR2A, in GnRH neurons appeared to be unchanged during this development.

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Section: Discussionsupporting

confidence: 51%

Expression of Glutamate Receptor Subunit mRNAs in Gonadotropin-Releasing Hormone Neurons during the Sexual Maturation of the Female Rat

Eyigor

Jennes²

1997

Neuroendocrinology

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“…Administration of the glutamate agonist NMDA induces precocious puberty in rats and nonhuman primates [57,428], while the antagonists MK-801 [563] and phencyclidine [501] delay puberty. Opinions differ as to whether this effect is mediated by kainate [161], NMDA, or dl-aamino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) [607] forms of the glutamate receptor [57], although stimulation of each receptor type has been shown to facilitate GnRH release [74,425]. Glutamate may not only stimulate GnRH release directly, but also indirectly via stimulating the release of the prostaglandin PGE 2 by local astrocytes, with this PGE 2 also facilitating GnRH release [389].…”

Section: Increases In Excitatory Tonementioning

confidence: 99%

The adolescent brain and age-related behavioral manifestations

Spear

2000

Neuroscience & Biobehavioral Reviews

4,688

110

4,301

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To successfully negotiate the developmental transition between youth and adulthood, adolescents must maneuver this often stressful period while acquiring skills necessary for independence. Certain behavioral features, including age-related increases in social behavior and risk-taking/novelty-seeking, are common among adolescents of diverse mammalian species and may aid in this process. Reduced positive incentive values from stimuli may lead adolescents to pursue new appetitive reinforcers through drug use and other risk-taking behaviors, with their relative insensitivity to drugs supporting comparatively greater per occasion use. Pubertal increases in gonadal hormones are a hallmark of adolescence, although there is little evidence for a simple association of these hormones with behavioral change during adolescence. Prominent developmental transformations are seen in prefrontal cortex and limbic brain regions of adolescents across a variety of species, alterations that include an apparent shift in the balance between mesocortical and mesolimbic dopamine systems. Developmental changes in these stressor-sensitive regions, which are critical for attributing incentive salience to drugs and other stimuli, likely contribute to the unique characteristics of adolescence. ᭧

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“…The pulsatile secretion and surge of LH depend on the activity of GnRH neurons (2). GnRH or LH secretion can be modulated by various inhibitory [endogenous opioids (3), cytokines (4), and inhibitory amino acids (5)] and stimulatory [catecholamines (6), neuropeptide Y (7), and excitatory amino acids (8)] modulators.…”

Section: T He Hypothalamic-pituitary-gonadal Axismentioning

confidence: 99%

Normal Suppression of the Reproductive Axis Following Stress in Corticotropin-Releasing Hormone-Deficient Mice*

et al. 1999

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The hypothalamic neuropeptide CRH has been postulated to inhibit LH secretion by a central action within the brain. To characterize the physiological significance of CRH in stressor-induced inhibition of LH secretion, CRH-deficient and wild-type mice were subjected to restraint or food withdrawal, and plasma LH levels were determined. The proestrus LH surge of female mice was equally suppressed by restraint in both genotypes, and central administration of a CRH antagonist did not alleviate this suppression in either genotype. Male mice of both genotypes also demonstrated suppression of both LH and testosterone secretion following restraint. Furthermore, food withdrawal caused similar suppression of LH secretion in both female and male mice regardless of CRH status. These data demonstrate that CRH is not necessary to inhibit LH secretion following either restraint or food withdrawal and that other molecules are able to suppress LH secretion during the response to stress in the context of CRH deficiency. (Endocrinology 140: 1702(Endocrinology 140: -1708(Endocrinology 140: , 1999 T HE HYPOTHALAMIC-PITUITARY-GONADAL AXIS in humans and rodents is maintained by the activity of GnRH neurons, whose cells are distributed throughout the preoptic region including the medial preoptic area (mPOA) of the anterior hypothalamus (1). The nerve terminals of these neurons project to the median eminence, where the release of GnRH into the hypophysial portal circulation occurs. The pulsatile secretion and surge of LH depend on the activity of GnRH neurons (2). GnRH or LH secretion can be modulated by various inhibitory [endogenous opioids (3), cytokines (4), and inhibitory amino acids (5)] and stimulatory [catecholamines (6), neuropeptide Y (7), and excitatory amino acids (8)] modulators.CRH has been proposed to negatively regulate GnRH secretion. An imbalance of central CRH has been implicated in the suppression of reproductive function in humans under stressful conditions. Patients with major depression or anorexia nervosa show suppressed reproductive function (9) and also have a high concentration of CRH in the cerebroventricular system (10). In rodents, intracerebroventricular (icv) administration of CRH attenuates GnRH level in the hypophysial portal circulation of female rats (11). Central, but not iv, injection of CRH also inhibits LH secretion over 5 h in a dose-dependent manner in ovariectomized female rats (12). These studies suggest a central inhibitory effect of endogenous CRH on the reproductive system, possibly acting upon GnRH neurons. Furthermore, 5 h of restraint, which activates the hypothalamic-pituitary-adrenocortical (HPA) axis and CRH gene expression (13), completely inhibits the proestrus LH surge and ovulation in intact cycling rats (14). Other stressors (undernutrition, hypoglycemia, or electric foot-shock) also inhibit LH secretion and pulsatility (15-17) as well as GnRH gene expression in the mPOA (18), and these effects are reversed following administration of a CRH antagonist in gonadectomized ...

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Differential effects of the N-methyl-d-aspartate and non-N-methyl-d-aspartate receptors of the excitatory amino acids system on LH and FSH secretion. Its effects on the hypothalamic luteinizing hormone releasing hormone during maturation in male rats

Cited by 28 publications

References 29 publications

Expression of Glutamate Receptor Subunit mRNAs in Gonadotropin-Releasing Hormone Neurons during the Sexual Maturation of the Female Rat

Expression of Glutamate Receptor Subunit mRNAs in Gonadotropin-Releasing Hormone Neurons during the Sexual Maturation of the Female Rat

The adolescent brain and age-related behavioral manifestations

Normal Suppression of the Reproductive Axis Following Stress in Corticotropin-Releasing Hormone-Deficient Mice*

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