Immunoreactive Gonadotropin-Releasing Hormone (Gn-RH) During Maturation in the Rat: Ontogeny of Regional Hypothalamic Differences

Araki, Shigeo; Toran-Allerand, C. Dominique; Ferin, Michel; Wiele, Raymond L. Vande

doi:10.1210/endo-97-3-693

Cited by 102 publications

(35 citation statements)

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“…This is in agreement with the observations of others [1,5,21]. By sampling at 2-day intervals we showed that the LHRH con tent did not change between 10 and 16 days of age.…”

Section: Discussionsupporting

confidence: 94%

In vitro Release of LHRH from the Hypothalamus of Female Rats during Prepubertal Development

Hompes¹,

Vermes

Tilders

et al. 1982

Neuroendocrinology

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In this study changes in serum FSH concentration, hypothalamic LHRH content and in vitro release of LHRH from hypothalami of female Wistar rats during prepubertal development are described. The concentration of FSH in serum was determined by radioimmunoassay. Extremely high levels (1.800 ng/ml) were found between 12 and 16 days of age. Thereafter, FSH levels rapidly fell to low levels (135 ng/ml) on day 32. LHRH was measured by radioimmunoassay in extracts of mediobasal hypothalami (MBH) and showed a gradual increase during the first 10 days of life. Between 10 and 16 days of age, hypothalamic LHRH content did not change. After day 16, LHRH content sharply increased to a maximum found on day 32. The release of LHRH from MBH of developing rats was studied during in vitro incubation in Krebs-Ringer bicarbonate buffer. LHRH in the medium was measured by radioimmunoassay. The spontaneous release rate of LHRH was maximal from MBH of 12-day-old rats and minimal from those of 32 days. Depolarization of neural membranes, by medium containing 45 mM K⁺ induced a stimulation of LHRH release. This K⁺-induced release of LHRH was also most prominent on day 12. These observations are consistent with the hypothesis that the high circulating FSH levels found in female rats between 12 and 16 days of age are at least in part caused by a high secretion rate of LHRH during this period.

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“…This is in agreement with the observations of others [1,5,21]. By sampling at 2-day intervals we showed that the LHRH con tent did not change between 10 and 16 days of age.…”

Section: Discussionsupporting

confidence: 94%

In vitro Release of LHRH from the Hypothalamus of Female Rats during Prepubertal Development

Hompes¹,

Vermes

Tilders

et al. 1982

Neuroendocrinology

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“…However, using a highly specific antiserum against GnRH and a very sensitive radioimmunoassay, Chiappa found measurable immunoreactive GnRH, although in very low concentrations, in hypothalamic extracts from rat fetuses from 15 days of gestation onwards. As in the study of Araki et al (1975), there was a progressive increase in hypothalamic GnRH content during post-natal development in male and female rats , although the GnRH content in females had decreased by the time of the first pro-oestrus. In a re-evaluation of the role of GnRH in the differentiation of gonadotrophs, Aubert et al (1985) detected immunoreactive GnRH in whole rat brain as early as 12 days of gestation.…”

Section: Gnrh and Gonadotroph Differentiation In The Fetussupporting

confidence: 61%

Role of GnRH in the maturation of pituitary gonadotroph function

Clayton¹

1985

Reproduction

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“…In the prepubertal rat, postnatal changes in the hypothalamic content of LHRH (16,17), neurotransmitter synthesis (18,19), and morphology of LHRH neurons (20) may represent functional maturation of various regulatory mechanisms for LHRH and the ingrowth of synaptic contacts. These events appear to be largely independent of gonadal steroids (21,22).…”

Section: Discussionmentioning

confidence: 99%

N‐Methyl‐DL‐Aspartate Receptor Antagonism by D‐2‐Amino‐5‐Phosphonovaleric Acid Delays Onset of Puberty in the Female Rat

Howe

Naylor

1990

J Neuroendocrinology

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To investigate the possible role of N-methyl-DL-aspartate (NMDA) receptor activation in the initiation of puberty, we examined the effects of the selective competitive antagonist 2-amino-5-phosphonovaleric acid (AP5) on the timing of vaginal opening. Paired and weight-matched litter mates of immature female rats were implanted with osmotic minipumps for the intracerebroventricular infusion of DL-or D-AP5 or artificial cerebrospinal fluid from 27 to 30 days of age for 14 days. Each animal was weighed and examined daily for vaginal opening as the indicator of first oestrous. Infusion of 20 or 40 mM DL-AP5 beginning on Day 30 failed to delay vaginal opening. Administration 50mM of the single enantiomer D-AP5 beginning on Day 27 significantly delayed the age of vaginal opening to 40.6f 1.1 (mean kSEM) days compared to the cerebrospinal fluid-infused controls (36.5k0.6 days). Blockade of NMDA receptors in the D-AP5-treated animals was confirmed on Day 32 by the suppression of luteinizing hormone response to intravenous NMDA (20 mglkg) while the response to exogenous luteinizing hormone-releasing hormone (50 nglkg) remained intact. AP5-treated animals had a slower rate of growth (3.1 +0.2 glday) compared to controls (4.2k0.2 glday). However, a similar degree of growth retardation produced by a 75% restricted diet in untreated juvenile animals did not delay vaginal opening. This suggests that the slower growth rate in the D-AP5-treated animals could not account for the delayed onset of puberty. In conclusion, these data suggest that blockade of central NMDA receptors inhibits excitatory mechanisms which may be important in the control of pubertal onset in the female rat.Puberty in the female rat can be regarded as a series of maturational events in the CNS associated with the gradual emergence of a s) nchronized pattern of pulsatile luteinizing hormone-releasing hormone (LHRH) secretion culminating in first ovultion (1). Although a decline in opioid-mediated inhibitory control can be demonstrated prepubertally (2, 3), recent evidence suggests that the formation or activation of excitatory neurotransmitter pathwaqs may be important in the control of the onset of puberty. Thus, pulsatile administration of N-methyl-DL-aspartate (NMDA), an agonist at NMDA receptors, is able to advance Pubcrty in juvenile animals (4).There is good evidence that NMDA acts to stimulate LHRH release in hypothalamic neurons; NMDA is without effect on gonadotrophs in v i m (5, 6); NMDA excites release of LHRH from hypothalamic explants in vitro (7) and in vivo NMDAstimulated LH secretion can be blocked by LHRH antagonists (8). That the specific NMDA antagonist, D-2-amino-5-phosphonovaleric acid (D-AP5), suppresses pulsatile LH secretion in adult castrates, at least acutely, suggests a role for endogenous excitatory amino-acid neurotransmitters in the control of LHRH secretion (9). It is therefore important to ascertain whether the endogenous ligands (glutamate and aspartate) are implicated in the mechanisms underlying the onset of pubert...

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Immunoreactive Gonadotropin-Releasing Hormone (Gn-RH) During Maturation in the Rat: Ontogeny of Regional Hypothalamic Differences

Cited by 102 publications

References 0 publications

In vitro Release of LHRH from the Hypothalamus of Female Rats during Prepubertal Development

In vitro Release of LHRH from the Hypothalamus of Female Rats during Prepubertal Development

Role of GnRH in the maturation of pituitary gonadotroph function

N‐Methyl‐DL‐Aspartate Receptor Antagonism by D‐2‐Amino‐5‐Phosphonovaleric Acid Delays Onset of Puberty in the Female Rat

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