Biomedical subjects

J I Koenig

Publications and source records attributed to J I Koenig.

At least 19 recordsLinked to original sources

PubMed2001

PreproTRH(178-199) and two novel peptides (pFQ7 and pSE14) derived from its processing, which are produced in the paraventricular nucleus of the rat hypothalamus, are regulated during suckling.

Suckling increases preproTRH messenger RNA in hypothalamic paraventricular neurons (PVN) and also markedly increases TRH release during the first period of lactation. Whether lactation alters preproTRH processing resulting in the generation of novel proTRH-derived peptides that may be involved in the regulation of PRL secretion lactation is not known. Therefore, in the present study we determine whether some other peptides derived from proTRH potentially contribute to lactation-induced PRL secretion. We have recently demonstrated that two members of the family of prohormone convertases PC1 and PC2 play a significant role in proTRH processing. PC1 is the major contributor in proTRH processing, whereas PC2 may have a specific role in cleaving TRH from its extended forms. In this study, we used a recombinant vaccinia virus system to coexpress rat preproTRH complementary DNA with PC1, PC2, and the neuropeptide 7B2 in GH4C1 cells (somatomammothophs, rat). We found that two novel peptides, preproTRH(178-184) (pFQ(7)), and preproTRH(186-199) (pSE(14)), were formed after the cleavage of their precursor preproTRH(178-199) (pFE(22)) by only PC2. Their formation was confirmed by microsequence analysis. Anatomical analyses revealed that these peptides are also found in the rat PVN. In addition, we found that pFE(22), pSE(14) and pFQ(7) produced a dose-dependent release of PRL from primary cultures of pituitary cells compared with one of the well studied secretagogues of PRL, TRH. To establish whether these peptides might play a role in vivo in the regulation of PRL release, we took rat litters on postnatal day 4, separated the pups from their mothers for 6 h, and then reunited the pups and mothers for 45 min. At the end of this period, the mothers were killed, acidic extracts of microdissected PVN were prepared and subjected to SDS-PAGE, followed by slicing and analysis by pFE(22) RIA. Forty-five minutes of suckling induced a marked 6-fold increase in serum levels of PRL. In addition, PVN levels of pFE(22) and pSE(14) increased approximately 5-fold during the same period in the acutely suckling females. Lactating animals that were separated from their litters and never reunited with their pups had low levels of PRL, and pFE(22) and pSE(14). These data provide the first evidence for alterations in proTRH processing in the PVN during lactation and suggest that the products of this altered processing may play a physiological role in the regulation of PRL secretion.

Animals↗

PubMed2000

Radiodetoxified lipopolysaccharide fails to activate the hypophyseal- pituitary-adrenal axis in the rat.

Lipopolysaccharide (LPS) is known to raise the concentration of the circulating stress hormones such as ACTH, corticosterone and beta-endorphin. This effect of endotoxin is mediated by different immune system-released hormone-like factors (e.g. interleukins, tumor necrosis factor etc.). Gamma-ray irradiation of LPS alters its biological properties and results in a radiodetoxified LPS preparation with numerous beneficial effects and decreased toxicity. In this study we compared the neuroendocrine effects of a commercial LPS and our native and radiodetoxified LPS preparations in rats. Plasma ACTH, corticosterone and beta-endorphin levels were measured by specific radioimmunoassays 120 min after intraperitoneal LPS administration. Control animals were injected with saline. Results show a dramatic increase in all hormones after administration of commercial and our native LPS preparation. Hormone levels in saline-injected controls and radiodetoxified LPS-treated rats did not rise significantly. These results suggest that radio-detoxification disintegrated that part of the LPS molecule complex which is responsible for toxicity including an enhanced production of cytokines, which trigger the hypothalamo-pituitary-adrenal axis.

Adrenocorticotropic Hormone↗

PubMed1999

Stimulation of anterior pituitary galanin and prolactin gene expression in suckling rats.

Recent evidence suggests that galanin may regulate prolactin (PRL) secretion during lactation. In this article, we describe the regulation of anterior pituitary galanin and PRL gene expression during pregnancy and after parturition in the rat. Expression of galanin and PRL in the anterior pituitary were significantly higher at d 20 of pregnancy compared to diestrus. One day after parturition, galanin mRNA levels increased a further 4.5-fold. This post partum increase in gene expression was not observed for PRL. The increase in galanin gene expression was maintained above the diestrous level for at least 10 d after parturition. PRL mRNA expression, on the other hand, was largely unchanged after parturition. Although the increase in galanin gene expression 1 d after parturition was independent of suckling, subsequently, galanin gene expression was significantly higher in nursing mothers. Anterior pituitary galanin gene expression was 12-fold higher in nursing mothers compared with those that were not, 3 d after parturition. Similarly, PRL gene expression was significantly lower in mothers who were not suckling their pups 3 d after parturition. Initiation of suckling alone was insufficient to stimulate galanin and PRL expression. Despite suckling for 2 d, removal of the suckling stimulus subsequently resulted in a rapid decrease in galanin gene expression. Hence, the stimulatory effect of suckling on galanin expression requires a sustained suckling stimulus. In conclusion, the data support the hypothesis that anterior pituitary galanin plays an important role during lactation, likely acting to amplify lactotroph stimulation through paracrine and autocrine mechanisms.

Aging↗

PubMed1998

Characteristics of the proopiomelanocortin system in the outdoor-bred domestic gander. II. Seasonal and circadian rhythmicity; effect of ether stress and lipopolysaccharide administration.

The responsiveness of the POMC system to exogenous stimuli and the diurnal and seasonal rhythmicity of ACTH and beta-endorphin (beta E) in plasma were studied in outdoor-reared domestic ganders. Plasma levels of ACTH- and beta E-like immunoreactivities were determined by direct and specific radioimmunoassays. In the first series of experiments immunoreactive (ir) ACTH and beta E were measured in the plasma of male domestic geese after 5 min of ether stress and after administration of 2 micrograms/kg lipopolysaccharide (LPS). Both ir-ACTH and ir-beta E levels increased 5 and 10 min after ether inhalation, but the increase in the ir-beta E concentration was only half that of the ir-ACTH. The plasma ir-ACTH levels were elevated after 60 and 120 min but not after 90 min of LPS administration: ir-beta E levels were unchanged at all time points. In a second series of experiments blood samples were taken on 30 March. 16 June, 4 August, and 27 October. On these days diurnal samplings were performed at 02:00, 06:00, 10:00, 14:00, 18:00, and 22:00 h. A two-way analysis of variance showed significant diurnal and seasonal changes for both hormones and significant interaction between the diurnal and seasonal levels. The highest daily mean values of the plasma ir-ACTH and ir-beta E concentrations were measured in June. The maximum of the ir-ACTH level was at 10:00 h in March and August, but at 22:00 h in June and October. The changes in ir-beta E concentrations paralleled those of ir-ACTH, but the changes did not reach statistical significance in every case.

Administration, Inhalation↗

PubMed1998

Characteristics of the proopiomelanocortin system in the outdoor-bred domestic gander. I. ACTH and beta-endorphin levels in the brain, pituitary, and plasma.

Immunoreactive (ir-) adrenocorticotropic hormone (ACTH) and beta-endorphin (beta E) levels were determined in seven brain regions, in the three pituitary lobes, and in the plasma of the domestic gander by specific radioimmunoassays. In the brain regions studied the relative concentrations of ir-ACTH and ir-beta E were the highest in the mediobasal hypothalamus and in the paraventricular nucleus. There were lower levels of these peptides in the supraoptic nucleus, in the septum, and in the dorsal thalamus. Very low ir-ACTH and -beta E contents were found in the archistriatum and in the lobus parolfactorius. In the pars distalis of the pituitary gland the cephalic lobe contained about 10 times more ir-ACTH (3596 pmol/lobe) and 4 times more ir-beta E (867 pmol/ lobe) than the caudal lobe (383 pmol/lobe and 189 pmol/lobe, respectively). Sephadex G-50 chromatography of pooled cephalic and caudal lobe extracts resulted in two distinct ir-beta E peaks, with elution volumes corresponding to the mammalian beta-lipotropin and beta E, and three ir-ACTH peaks, the second one coeluting with mammalian ACTH. In the neural lobe the ir-ACTH/-beta E concentrations were similar to those in the hypothalamus. Resting plasma ir-ACTH (12.8 +/- 1.47 pmol/ml) but not ir-beta E (31.4 +/- 1.22 pmol/ml) levels were significantly increased following castration (to 41.4 +/- 1.11 pmol/ml). Serial blood sampling indicated pulsatile ir-beta E secretion (mean, coefficients of variation, and minimum-maximum range: 17.5, 62.78, and 2.9-49.7, respectively, for gander 1 and 23.3, 62.85, and 5.00-61.5, respectively, for gander 2).

Adrenocorticotropic Hormone↗

PubMed1998

Increase in plasma leptin and Lep mRNA concentrations by food intake is dependent on insulin.

Obese (Lep) gene expression and leptin secretion are regulated by changes in food intake. However, the mechanism by which leptin concentrations are altered by fasting and feeding is unclear. Since these changes occur in parallel with changes in plasma insulin, it is possible that the changes observed are mediated by insulin. To test this hypothesis, we studied the role of insulin in the regulation of Lep gene expression in epididymal fat and leptin secretion during feeding. As shown previously, fasted animals showed significant reductions in Lep mRNA, plasma leptin, and plasma insulin concentrations. Conversely, feeding increased plasma insulin, Lep mRNA, and plasma leptin. In streptozotocin (STZ)-treated animals, plasma insulin concentrations were low. This was associated with low Lep mRNA and plasma leptin concentrations. Changes in food intake, whether fasting or feeding, did not significantly alter plasma insulin levels in STZ-treated animals. Under these circumstances, Lep mRNA and plasma leptin concentrations also remained low. Our results demonstrate that the decrease in Lep mRNA and plasma leptin during fasting and the increase with feeding are dependent on changes in the plasma insulin concentration.

Animal Feed↗

PubMed1998

Regulation of leptin expression and secretion by corticosteroids and insulin. Implications for body weight.

Leptin is an important hormone that has potent effects on appetite and body weight. The regulation of leptin gene expression and secretion by corticosteroids and insulin was studied in the rat. Adrenalectomy resulted in a significant reduction in leptin gene expression and secretion. The reduction was corrected by hormonal replacement with corticosterone pellets, showing that normal levels of circulating corticosteroids are required to maintain leptin expression and secretion in the body. Chronic treatment with dexamethasone (DEX) over 3 wk did not significantly increase leptin gene expression and secretion, contrary to earlier reports using shorter treatment paradigms. The profound weight loss associated with chronic DEX treatment may have abrogated the direct stimulatory effect of DEX on leptin gene expression and secretion, indicating a possible crosstalk between corticosteroids and leptin in the regulation of body weight. Shorter-term treatment of animals with DEX (3.7 micrograms/g body wt; 24 h) increased leptin gene expression and secretion about 2-fold and 1.4-fold, respectively. The increase was independent of circulating insulin concentrations. In streptozotocin-treated rats, short-term DEX treatment increased leptin gene expression and secretion about 3.5-fold and 2-fold, respectively. The data indicate that circulating leptin concentrations and adipose tissue leptin expression are dependent on corticosteroids and insulin. Although acute DEX treatment resulted in a stimulatory effect on leptin secretion and expression, chronic DEX treatment did not. The stimulatory effect of DEX on leptin is independent of circulating insulin concentrations.

Adipose Tissue↗

PubMed1997

Regulation of anterior pituitary galanin gene expression by thyroid hormone.

Thyroid hormone is required for basal and estrogen-induced expression of anterior pituitary galanin. Steady-state anterior pituitary galanin mRNA levels decreased 6-fold in hypothyroid rats after 3 weeks of treatment. Similarly, hypothyroidism resulted in a 2.6-fold decrease in estrogen induction of galanin gene expression. The effect of thyroid hormone on anterior pituitary galanin gene expression appears to be exerted, at least in part, at the pituitary itself. Transient expression assays in GH3 cells suggest the involvement of transcriptional mechanisms in the regulation of galanin gene expression by thyroid hormone. A region between -41 and -132 bp upstream of the transcriptional start site confers thyroid hormone responsiveness to the galanin gene. Gel-mobility shift assays show specific binding of 'SPI-like' proteins in GH3 nuclear extracts to this region of the galanin gene. This binding was greatly enhanced by thyroid hormone.

Animals↗

PubMed1997

Effects of anterolateral and posterolateral cuts around the medial hypothalamus on the immunoreactive ACTH and beta-endorphin levels in selected brain regions of the rat.

To evaluate the relative weight of the ACTH-ergic and beta-endorphin-ergic pathway(s) leaving the medial hypothalamus (MH) in anterior or posterior directions immunoreactive ACTH and beta-endorphin (ir-ACTH and ir-betaE) were quantified in selected brain regions of the rat 7-8 days after placing anterolateral (ALC) or posterolateral (PLC) cut around the MH. Retrograde accumulation of both peptides was observed in the MH after ALC, but not after PLC. ALC resulted in dramatic decrease in ir-ACTH/ir-betaE concentrations in all extra-MH brain regions tested (extra-MH hypothalamus, septum, thalamus, hippocampus, amygdala, and medulla oblongata). In contrast, ir-ACTH and ir-betaE levels decreased only in the thalamus and in the medulla oblongata after PLC. The present data indicate (a) ACTH- and betaE-like substances synthesized in the arcuate region of the hypothalamus are axonally transported to extrahypothalamic brain regions by neuronal pathways leaving the MH primarily anterolateral, anterodorsal, or anteromedial direction (even the fibers of certain posteromedial or posterolateral projections leave the MH some anterior directions); (b) the posterior ACTH-/betaE-ergic projections seem to be of minor importance except for the thalamus and the medulla oblongata where it contributes to about one-third of the peptide content. Our biochemical study provide quantitative complementary data to the detailed immunohistochemical picture of the ACTH/betaE-ergic projections in the rat brain described by Khachaturian et al.

Adrenocorticotropic Hormone↗

PubMed1997

Age-dependent muscarinic stimulation of beta-endorphin secretion from rat neurointermediate lobe in vitro.

The effect of acetylcholine on the neurointermediate lobe beta-endorphin secretion was studied in the neonatal and in the adult rat in vitro. Acetylcholine stimulated beta-endorphin secretion from the 2-day- and 5-day-old neurointermediate lobe, the effect was dose dependent and more pronounced in the presence of the cholinesterase inhibitor eserine. The 10-day-, the 21-day-old and the adult rat neurointermediate lobes did not respond to acetylcholine, even in the presence of eserine. Basal beta-endorphin secretion was elevated by the D2 receptor antagonist sulpiride, but acetylcholine was without effect in the 10-day-old and in the adult neurointermediate lobe even after dopamine receptor blockade. The beta-endorphin stimulatory response to acetylcholine was diminished by the M1 muscarinic receptor antagonist pirenzepine and blocked by the M3 > M1 antagonist 4-diamino-phenyl-piperidine (4-DAMP). The selective M2 antagonist methoctramine and nicotine had no effect. These data indicate that the neurointermediate lobe beta-endorphin secretion is under special muscarinic cholinergic regulation for a relatively short time after birth. The disappearance of this stimulatory cholinergic effect in later life might be due to changes in the intracellular secretory machinery in the IL and/or to the uncoupling of the cholinergic receptors from the intracellular signal transduction system(s) responsible for the stimulated secretion in the rat melanotrope cells.

Acetylcholine↗

PubMed1996

Temporal changes in insulin-like growth factor I, c-fos, and c-jun gene expression during hyperplastic kidney growth in weanling rats.

We have previously determined that compensatory renal growth (CRG) during the initial 24-48 h after uninephrectomy (UNX) is GH independent in weanling animals, but associated with significant increases in insulin-like growth factor I (IGF-I) and IGF-I receptor gene expression. The purpose of the present study was to determine the temporal sequence of molecular and cellular events that occur at various time points (1, 6, 12, 18, 24, 48, and 72 h post-UNX) during this early period of accelerated renal growth in the weanling (21- to 25-day-old) rat. Rapid and sustained increases in steady state renal IGF-I receptor and IGF-I messenger RNA (mRNA) were observed at 1 and 6 h, respectively, and remained elevated in the remnant kidneys until 72 h post-UNX. The mRNAs for the early response genes, c-fos and c-jun, were not induced in the remnant kidneys from weanling rats until between 12-18 h, but were also sustained through 48 h post-UNX. Increases in remnant kidney DNA content and [3H]thymidine incorporation also occurred from 18-48 h post-UNX and returned to baseline levels by 72 h post-UNX, indicating that the hyperplastic response in the weanling remnant kidney occurs over a discrete period early after UNX. Neither IGF-I nor early response genes were elevated in kidneys from adult animals, which exhibited only hypertrophic renal growth at those early time points after UNX. These findings suggest that early CRG in the weanling rat is associated with rapid increases in IGF-I mRNA followed by a rise in c-fos and c-jun gene expression and a mitogenic response. Furthermore, when the mRNA levels of IGF-I and early response genes returned to baseline levels, mitogenic growth stopped, and slower prolonged hypertrophic renal growth ensued.

Animals↗

PubMed1995

Adrenocorticotropin, prolactin and beta-endorphin stimulatory actions of alpha-2-adrenoceptor antagonists.

We studied the effect of glucocorticoid pretreatment, mediobasal hypothalamus lesion (MBHL) and the interaction between clonidine and yohimbine in male Wistar rats to elucidate the sites and/or mechanisms of endocrine actions of alpha 2-antagonists. The pretreatment of 1 mg/kg s.c. dexamethasone for 4 days effectively prevented the stimulatory effect of alpha 2-antagonists yohimbine (5 mg/kg i.p.) and CH-38083 (1 mg/kg i.p.) on adrenocorticotropin (ACTH) secretion, while the action of these antagonists on prolactin (PRL) and beta-endorphin (beta E) remained unchanged. The central (i.c.v.) pretreatment of 5 micrograms/rat clonidine failed to antagonize the prolactin (PRL) and beta E releasing effect of yohimbine. However, it inhibited the yohimbine-induced ACTH secretion. MBHL resulted in a significant enhancement in basal plasma PRL and beta-endorphin (beta E) levels. But basal plasma ACTH levels have not been changed. Yohimbine failed to stimulate ACTH secretion in MBH-lesions rats, while PRL and beta E response to the yohimbine was maintained in these animals. This study confirms that the alpha 2-antagonists stimulate ACTH secretion by a corticosteroid-sensitive mechanism which is located centrally. In contrast, alpha 2-antagonists affect PRL and beta E secretion via a corticosteroid-insensitive mechanism located at the periphery, possible within the pituitary gland.

Adrenergic alpha-2 Receptor Antagonists↗

PubMed1995

Effect of interleukin-1 beta on plasma ACTH, beta-endorphin, and corticosterone levels in infant and prepubertal rats.

IL-1 beta is known to enhance ACTH release from the anterior pituitary in the adult rat, mainly by simulating the hypothalamic ACTH-releasing hormone (CRH) release, but it seems to have a direct effect on the pituitary and on the adrenal hormone secretion, too. The effect of IL-1 beta on the beta-endorphin (beta E) secretion from the intermediate lobe is less well studied. There is very little information on the effect of IL-1 beta on the hypothalamic-pituitary-adrenal axis (HPAA) in the postnatal rat, which is a special period, because the reactivity of the HPAA is blunted. The effect of IL-1 beta in this period seemed to be of special interest, because neither the immune nor the endocrine system is fully developed. In the present study we tested the 30- and 120-min effect of intraperitoneally administered 0.5 and 100 ng/g body weight IL-1 beta on the plasma immunoreactive (ir) ACTH, beta E, and corticosterone (CS) levels in the 10-d-old (infant) and 30-d-old (prepubertal) rat. Generally, the ir-ACTH, ir-beta E, and ir-CS levels were significantly higher in prepubertal than in infant rats. Hormone levels were more enhanced by the higher dose of IL-1 beta, and changes were more pronounced at 120 min than at 30 min. The relative increase of ir-ACTH and ir-beta E was smaller in the infant than in the prepubertal rat. In contrast, the relative increase of ir-CS was more pronounced in the infant rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1994

Galanin-containing neurons in the paraventricular nucleus: a neurochemical marker for fat ingestion and body weight gain.

The physiological function of the peptide galanin (Gal) remains to be established. It is known to exist in high concentrations within the hypothalamus and to modulate the secretion of specific hormones, as well as to potentiate food consumption. Our study provides evidence for an essential function of neuronal Gal, within a specific hypothalamic area, in stimulating the behavioral process of fat ingestion and body weight gain. Through analyses of peptide levels via RIA and of gene expression via in situ hybridization, a close positive association is established between Gal in the paraventricular nucleus (PVN), particularly its midlateral region, and fat ingestion. No such relationship is detected for Gal in other brain areas or between PVN Gal and ingestion of carbohydrate or protein, supporting the behavioral and anatomical specificity of this relationship. Through PVN injection studies with antisense oligonucleotides to Gal mRNA, a dramatic decline in fat ingestion and body weight suggests that endogenous Gal contributes to the natural appetite for fat. Thus, Gal in the PVN is identified as a neurochemical marker for fat ingestion and, consequently, body weight gain.

Analysis of Variance↗

PubMed1994

Adrenalectomy alters discrete galanin mRNA levels in the hypothalamus and mesencephalon of the rat.

Using solution and in situ hybridization techniques we have studied the effects of adrenalectomy with or without restitution therapy with corticosterone on galanin mRNA levels in discrete regions of the male rat brain. Galanin peptide levels were also measured using a radioimmunoassay. The solution hybridization showed a two-fold increase in galanin mRNA 7 days, but not 14 days, after adrenalectomy in the preoptic area including the hypothalamic paraventricular nucleus (PVN). No changes were observed in the mediobasal hypothalamus including the arcuate nucleus. In situ hybridization showed that the increase in galanin mRNA was localized to the PVN and that the arcuate nucleus was not affected. The changes observed could be fully counteracted by corticosterone treatment. Radioimmunoassay showed decreased galanin levels in the median eminence 14 days, but not 7 days, after adrenalectomy and increased levels in the anterior pituitary and neurointermediate lobe. The results give evidence for a regional regulation of galanin gene expression and galanin peptide synthesis by adrenocortical steroids.

Adrenalectomy↗

PubMed1994

Diurnal rhythm of galanin-like immunoreactivity in the paraventricular and suprachiasmatic nuclei and other hypothalamic areas.

The peptide galanin (GAL), when injected into the rat hypothalamus, is known to stimulate feeding behavior and affect the secretion of various hormones, including insulin and the adrenal steroid, corticosterone. To determine whether endogenous peptide levels shift in relation to natural rhythms of feeding and circulating hormone levels, rats were sacrificed at different times of the light/dark cycle, and their GAL levels were measured, via radioimmunoassay, in medial hypothalamic dissections and micropunched hypothalamic areas. The results suggest the existence of two distinct diurnal rhythms for hypothalamic GAL. One rhythm, detected exclusively in the area of the SCN, is characterized by bimodal peaks of GAL, threefold higher than basal peptide levels, around the onset of the dark and light periods. The second rhythm shows a single peak of GAL towards the middle of the nocturnal feeding cycle, specifically between the third and sixth hour. This latter rhythm is evident in the dorsal region of the medial hypothalamus, localized specifically to the lateral portion of the PVN. Moreover, it is inversely related to circulating insulin but unrelated to the adrenal steroids, suggesting a possible association between this pancreatic hormone and GAL in the PVN.

Aldosterone↗

PubMed1993

Estrogen stimulation of galanin gene expression and galanin-like immunoreactivity in the rat and its blockade by the estrogen antagonist keoxifene (LY156758).

Rat galanin (rGAL) gene expression is stimulated potently by 17 beta-estradiol in the anterior pituitary. Neuroendocrine tissue extracts of were purified by chromatography and analyzed for rGAL-like (-LI) immunoreactivity. Greater than 90% of rGAL-LI eluted at the same position as the synthetic rGAL standard in untreated anterior pituitary, median eminence and neurointermediate lobe tissues. Additional immunoreactive forms were detected in the hypothalamus, anterior pituitary and MtT/W15 adenoma tissues, particularly after 17 beta-estradiol treatment. We examined rGAL and its encoding mRNA in the anterior pituitary of immature female rats after the injection of pregnant mare serum gonadotropin (PMSG). One and two days after PMSG injection, serum 17 beta-estradiol increased 3-fold and 4-fold, respectively. This resulted in a surge of endogenous gonadotropin 2 days after PMSG. At this time, rGAL-encoding mRNA was increased 40-fold over controls. Three days after PMSG, there was a 6-fold increase in anterior pituitary and a 41% increase in plasma rGAL-LI concentrations. Plasma 17 beta-estradiol one day after injection of PMSG and the consequent anterior pituitary rGAL-LI concentrations 2 days later were positively correlated. This stimulation of rGAL and its encoding mRNA by PMSG was inhibited by treatment with the estrogen antagonist keoxifene (LY156758).

Adenoma↗

PubMed1993

Effects of Hypnorm (fentanyl) on ACTH/beta-endorphin levels in plasma, pituitary and brain of 10-day old rats.

Administration of Hypnorm, an anaesthetic containing the known mu-opiate receptor agonist fentanyl, elicited dose- and time-related elevation of plasma ACTH, beta-endorphin and corticosterone levels in 10-day old rat pups. Pretreatment with specific antibodies (raised against CRH, AVP and ACTH resp.) revealed that Hypnorm administration activated the ACTH-corticosterone system in the 10-day old rat and its effect is mediated by CRH and/or AVP. Hypnorm anaesthesia was associated with significant decrease in the ACTH and beta-endorphin levels in the pituitary lobes as well as in beta-endorphin content of the hypothalamus and medulla oblongata. Latter results may indicate that the beta-endorphinergic system in the brain of the 10-day old rat is activated by Hypnorm, an effect most probably elicited by the opiate agonist fentanyl.

Adrenocorticotropic Hormone↗