The present experiments investigated the time course of maternal modulation of GH secretion and examined the possible role of milk in the regulation of GH secretion in neonatal rats. Serum GH concentrations in neonatal rats were high at birth and declined over time postpartum. Separation of rat pups from their mothers decreased, while a subsequent period of suckling increased, serum GH levels in rat pups on postpartum days 1-14, but not on day 20. The water-soluble fraction (infranatant) of rat milk contained immunoreactive (ir) rat GH-releasing hormone (rGHRH)-like material (725.06 +/- 81.29 pg/ml), ir-somatostatin-like activity (1.64 +/- 0.2 ng/ml), and irGH (4.79 +/- 0.73 ng/ml). The concentrations of these hormones tended to decrease with time postpartum and were positively correlated with each other (r = 0.70; P less than or equal to 0.0001). IrPRL was also present in the infranatant (148.44 +/- 14.55 ng/ml), but levels were not correlated with the other hormones detected. Milk infranatant stimulated GH secretion from perifused neonatal rat pituitary glands in vitro. Milk infranatant also stimulated GH secretion in vivo when administered sc or intragastrically to 2- or 8-day-old rat pups. The GH-releasing effect was not due to gastric distension or nonspecific nutritive components, as neither 0.9% saline nor nutrients (5% glucose and 10% BSA) increased serum GH levels. The presence of high concentrations of irGHRH in rat milk infranatant and the strong correlation between the irGHRH concentrations of milk samples and the in vitro GH response (r = 0.71; P less than or equal to 0.005) suggested that this peptide is a major candidate for producing the in vitro and in vivo GH-stimulating activity in rat milk. However, the minimally effective concentration of synthetic rGHRH required to stimulate GH release in the superfusion system was between 1-10 nM, which exceeds milk irGHRH levels by 100- to 1000-fold. Moreover, in vivo administration of synthetic rGHRH (sc or intragastrically) was unable to increase serum GH concentrations in 2-day-old pups, although a large dose (100 ng/g) of human GHRH sc was effective. These findings indicate that rat milk may be an important maternal factor that modulates GH secretion and, consequently, growth during the neonatal period. Rat milk has GH-releasing activity both in vivo and in vitro in neonatal rats, but the GH-releasing activities of milk are probably only minimally due to its rGHRH content.
The mechanism by which estrogen enhances prolactin (PRL) secretion and induces hyperplasia of lactotrophs is not defined clearly. The objective of this study was to examine hypothalamic monoaminergic PRL regulatory systems and pituitary hormone secretion in the early and later stages of estrogen-induced hyperprolactinemia and pituitary hyperplasia. Dopamine (DA) and serotonin (5-HT) turnover were determined in microdissected brain regions 3 and 30 days after a single subcutaneous dose of estradiol (2 mg) to male ACI rats. Plasma samples were collected in animals with indwelling intra-atrial cannulae. 3 days after estrogen there was a significant increase in plasma PRL, pituitary PRL and growth hormone (GH), and DA turnover in the median eminence and arcuate nucleus. Plasma concentrations and pituitary content of PRL increased at 30 days. The responsiveness of PRL to thyrotropin-releasing hormone (TRH) was enhanced at both times. Concentrations of DA decreased considerably in the median eminence and arcuate nucleus by 30 days, and turnover decreased in the median eminence. 5-HT turnover was not affected in the early stages of hyperprolactinemia. Plasma GH increased and TSH was unchanged, even though pituitary content of both hormones decreased at 30 days. Estrogen had no effect on plasma corticosterone. These findings support the hypothesis that estrogen induces pituitary hyperplasia by antagonizing DA inhibition of PRL-secreting cells and by enhancing their responsiveness to TRH.
Somatostatin inhibits growth hormone (GH) and thyrotropin (TSH) secretion in the rat. Previous studies have shown that small discrete lesions of the periventricular hypothalamic (PV) and medial-basal amygdaloid (AMG) nuclei, which contain high concentrations of somatostatin neurons, reduce somatostatin-like immunoreactivity (SLI) in the median eminence (ME) by approximately two thirds and one third, respectively. The present study assessed the function of the PV and AMG somatostatin systems in the regulation of basal episodic GH and TSH secretion. Three experiments were performed in freely behaving, chronically cannulated adult male rats. In experiment 1, bilateral electrolytic lesions (20 mC) were placed in the PV at the level of the paraventricular nucleus. In experiment 2, bilateral thermal lesions (55 °C × 1 min) were placed in the AMG. In experiment 3, thermal lesions were placed in both the PV and AMG (PV/AMG). Blood samples were removed from animals every 15 min for 5.5 h 14–21 days postoperatively. The ME was microdissected for determination of SLI content. PV, AMG and PV/AMG lesions reduced ME SLI by 59, 26, and 91%, respectively. PV or AMG lesions had no effect on the amplitude or frequency of GH secretory peaks, GH trough levels or the total amount of GH secreted, whereas combined PV/AMG lesions reduced GH peak levels. Lesions of the AMG caused a 34% increase in mean plasma TSH levels, while PV or PV/AMG lesions reduced TSH. The latter effect was probably caused by damage to thyrotropin-releasing hormone neurons and/or axons, which are also located in the PV region. These results suggest that PV and AMG somatostatin systems may not have a significant role in the regulation of basal episodic GH secretion and the putative AMG somatostatin system exerts a significant inhibitory influence on TSH secretion.
In the present investigation CNS epinephrine (EPI) biosynthesis was selectively interrupted with specific norepinephrine N-methyltransferase (NMT) inhibitors, SK&F 64139 (Smith, Kline & French Laboratories) and LY 78335 (Eli Lilly & Co. Research Laboratories), to determine the effects of central EPI depletion on basal and cold, thyrotropin-releasing hormone, and hypothalamic somatostatin antiserum induced thyrotropin (TSH) secretion in chronically cannulated rats. Because these NMT inhibitors also are α2-adrenergic receptor blockers, the effects of α2- and α1-adrenergic blockade and α2-activation on plasma TSH were assessed with rauwolscine and corynanthine and B-HT933, respectively. Serum T4 and plasma corticosterone were also measured. Blockade of CNS EPI synthesis resulted in inhibition of basal and cold and thyrotropin-releasing hormone induced TSH release, suppression of serum T4, and increased corticosterone release. The stimulatory effect of SRIF antiserum on plasma TSH was not altered by SK&F 64139. α2-adrenergic blockade suppressed plasma TSH levels, but not to the same degree as the NMT inhibitors; activation of α2-receptors enhanced TSH secretion. Thus, it is possible that part of the effect of the NMT inhibitors on TSH was due to α2-blockade. α1-adrenergic blockade also lowered plasma TSH. These results indicate that (1) central EPI systems have a stimulatory role in TSH regulation, possibly mediated by α2-adrenergic receptors, (2) cold-induced TSH release is mediated, in part, by EPI, and (3) central EPI systems exert an inhibitory effect on the hypothalamic-pituitary-adrenal axis.
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