bluuebunny/crossref_metadata_2025_split huggingface dataset:
Investigation of the ontogenetic patterns of rat hypothalamic dopaminergic neurone morphology and function in vitro
Authors: Murray H. E. , Gillies G. E. 
Published: December 2008

ABSTRACT
Using fetal rat hypothalamic cells in primary culture maintained in a serum-free defined medium we have investigated the morphological and functional development of the dopamine (DA)-containing neurones intrinsic to the hypothalamus.
Immunocytochemical studies demonstrated the presence of three morphologically distinct subtypes of tyrosine hydroxylase-immunopositive neurones. On day 3 in vitro unipolar, bipolar and multipolar cell types were apparent. The latter two subtypes persisted to later days in culture and increased both in perikarya size and neurite length. All subtypes have been shown to have correlates in vivo.
Biochemical studies employing [3H]DA demonstrated a time- and temperature-dependent uptake mechanism within the cultures which was significantly attenuated by the uptake inhibitors benztropine and nomifensine in a dose-dependent manner. [3H]DA was also released under both basal and 56 mmol K+/l-stimulated conditions and the magnitude of the response was reduced by exclusion of calcium from the release medium. The amount of [3H]DA accumulated and released by the cultured cells increased with the age of the culture, suggesting functional maturation of the DA-containing neurones within this preparation.
The role of oestradiol-17β in regulating hypothalamic dopaminergic function was also investigated both indirectly with the use of [3H]DA and by direct measurement of endogenously synthesized DA using high-performance liquid chromatography coupled with electrochemical detection. Both uptake and release of [3H] and release of endogenous DA were significantly modulated by the concentration of steroid in the defined medium.
These results demonstrate that hypothalamic dopaminergic neurones, when maintained in primary culture, undergo morphological and functional maturation which have several correlates in vivo. In addition, we have demonstrated that at least one sub-population of dopaminergic neurones within this preparation is responsive to oestradiol-17β.
As DA is considered to be a vital component in the regulation of neuroendocrine activity we suggest that this model is valuable for the investigation of the functional development of the DA systems of the hypothalamus and the relationship existing between neurotransmitters, neuropeptides and neuroactive steroids.
Journal of Endocrinology (1993) 139, 403–414
A modulatory role of endogenous opioids on prolactin secretion at the end of pregnancy in the rat
Authors: Soaje M , Deis R P 
Published: December 2008

Abstract
It is well known that the fall in serum progesterone concentrations during late pregnancy induces prolactin secretion in rats. On day 19 of pregnancy, administration of 10 mg of the antiprogesterone RU-486/kg induced a small but significant increase in serum prolactin. A lower dose (2 mg/kg) was not effective. Administration of naloxone (2 mg/kg) to pregnant rats on day 19 of pregnancy did not modify circulating prolactin but, after RU-486 treatment, a notable increase in serum prolactin was obtained 30 min after naloxone was given. The lack of effect of naloxone-methobromide in pregnant rats pretreated with RU-486 may indicate that the opioid-induced prolactin suppression acts centrally, most probably at the hypothalamic level. During day 21 of pregnancy, the time-course of prolactin secretion, measured at 0900, 1400, 1900 and 2200 h, was inversely correlated with circulating progesterone levels. At 0900 h, serum prolactin was very low with high serum progesterone concentrations but a significant increase in serum prolactin occurred at 2200 h; this was coincident with a significant decrease in the steroid. The stimulatory effect of naloxone on prolactin secretion was clearly dependent on the circulating progesterone level. Thus, at 1900 h of day 21, naloxone induced a significant increase in serum prolactin but, at 2200 h, the opioid antagonist dramatically enhanced the circulating level of prolactin. The serum prolactin increase induced by naloxone at 1900 h was prevented by the s.c. administration of 5 mg progesterone given 7 h earlier. Similarly, the large increase in serum prolactin levels at 1800 h on day 19 of pregnancy, after administration of RU-486 plus naloxone, was completely abolished by treatment with CB154. The lack of effect of RU-486 and naloxone on serum prolactin levels in virgin rats on the day of pro-oestrus demonstrates that the effect of naloxone on prolactin in pregnant rat is peculiar to the end of pregnancy.
In conclusion, the attenuation of the central inhibitory action of progesterone facilitates the release of prolactin which is dramatically enhanced by naloxone treatment. These results provide an important new insight into the existence of a neuromodulatory regulation of prolactin secretion by the opioid system showing a paradoxical opioid-induced prolactin suppression at the end of pregnancy.
Journal of Endocrinology (1994) 140, 97–102
Lipopolysaccharide modulation of eicosanoid and corticotrophin-releasing hormone release from rat hypothalamic explants and astrocyte cultures in vitro: evidence for the involvement of prostaglandin E2 but not prostaglandin F2α and lack of effect of nerve growth factor
Authors: Pozzoli G , Costa A , Grimaldi M , Schettini G , Preziosi P , Grossman A , Navarra P 
Published: December 2008

Abstract
Bacterial lipopolysaccharide (LPS) and prostaglandins (PG) E2 and F2α are putative activators of the hypothalamo-pituitary-adrenal axis. Certain of the biological effects of LPS may be mediated by cytokines such as interleukin-1β (IL-1β), while IL-1β itself may operate via induction of the prostaglandins and/or nerve growth factor (NGF). As IL-1β stimulates the release of corticotrophin-releasing hormone (CRH) from acute rat hypothalamic explants directly, the effects of these substances on the release of CRH in vitro were investigated in short- and medium-term (20 and 60 min) incubations. The effect of LPS on the release of PGE2 and PGF2α from these explants, as well as from cortical astrocyte cultures, was also studied.
LPS did not modify the release of CRH, PGE2 or PGF2α in 20-min incubations. In 60-min incubations, LPS stimulated the release of PGE2, whereas the release of CRH was weakly, but significantly, reduced; PGF2α was not altered. PGE2 significantly stimulated CRH release in the 60-min but not in the 20-min experiments. This effect appeared to be selective for PGE2, since PGF2α did not modify CRH release, alone or in combination. LPS also selectively released PGE2 but not PGF2α from cortical astrocyte cultures after 24-h incubation. NGF had no effect on the release of explant CRH, regardless of the length of incubation.
It was concluded that neither LPS nor NGF acutely stimulate the hypothalamo-pituitary-adrenal axis by a direct action on hypothalamic CRH, while hypothalamic PGE2 may mediate, at least in part, certain of the neuroendocrine responses to LPS.
Journal of Endocrinology (1994) 140, 103–109
Long-term changes of somatotrophic function induced by deprivation of growth hormone-releasing hormone during the fetal life of the rat
Authors: Cella S G , Locatelli V , Broccia M L , Menegola E , Giavini E , De Gennaro Colonna V , Torsello A , Wehrenberg W B , Müller E E 
Published: December 2008

Abstract
We have studied the effects of intra-amniotic administration of an anti-GH-releasing hormone serum (GHRH-Ab) on day 16 of fetal life in the rat, when the ontogenetic development of the GHRH neuronal system occurs. Control animals received normal rabbit serum. Following delivery, body weight was monitored for the next 30 days as an index of somatic growth, and the following indices of somatotrophic function were determined: plasma and pituitary GH, pituitary GH mRNA, hypothalamic GHRH and somatostatin mRNA, and the in vivo GH responsiveness to GHRH. At birth, GHRH-Ab-treated rats had a body weight that was equivalent to that of control rats but, starting from postnatal day 6 up to day 30, they had a significantly reduced body weight. Pituitary weight, the absolute pituitary GH content and GH mRNA levels were lower in experimental compared with control rats, while pituitary GH concentrations were similar in the two groups, thus implying that there was a defect, not only in GH synthesis, but also in GH release. In agreement with this theory, basal GH levels and GHRH-stimulated GH secretion were reduced in GHRH-Ab-treated rats but, in contrast, hypothalamic regulation of GH secretion appeared to be working in these rats as they were still able to respond to the low plasma GH by increasing GHRH and decreasing somatostatin mRNA levels. These findings indicate that deprivation of GHRH during fetal life induces long-lasting changes of growth rate and somatotrophic function. In addition, when comparing these changes with those in rats given GHRH-Ab postnatally, it would appear that deprivation of GHRH affects different regulatory levels of the hypothalamo-pituitary-somatotroph axis depending on when the deprivation occurs.
Journal of Endocrinology (1994) 140, 111–117
Increased insulin receptor number and insulin responsiveness in a chicken hepatoma cell line
Authors: Taouis M , Derouet M , Caffin J P , Simon J 
Published: December 2008

Abstract
Insulin receptor number and insulin responsiveness were compared in a chicken hepatoma cell line (LMH) and in normal chicken hepatocyte (cHep) cells cultured in the same conditions. LMH cells expressed two- to threefold more insulin receptors than cHep cells, without significant changes in affinity. The tyrosine kinase activity of solubilized and lectin (lentil+wheat germ agglutinin; WGA)-purified LMH receptors was higher than that of cHep receptors. The ATP hydrolytic activity previously observed in WGA-purified receptors from chicken liver membranes was also present in WGA-purified receptors from cultured cHep cells. This unidentified membrane-associated ATPase was absent from LMH membrane-solubilized material and therefore from WGA-purified LMH insulin receptors. Finally, LMH cells incorporated at least tenfold more amino isobutyric acid than cHep cells in the absence of insulin and were more responsive to insulin. The enhanced basal amino acid transport of LMH cells was most probably the consequence of their proliferative activity. The enhanced insulin responsiveness of LMH cells can be accounted for, at least in part, by one or several of the modifications presently demonstrated in LMH cells when compared with normal cultured hepatocytes: increased insulin receptor number and tyrosine kinase activity and possibly the loss of the membrane-associated ATPase.
Journal of Endocrinology (1994) 140, 119–124
Low intrathyroidal iodine concentration in non-endemic human goitres: a consequence rather than a cause of autonomous goitre growth
Authors: Aeschimann S , Buergi U , Wagner H E , Kaempf J , Lauber K , Studer H 
Published: December 2008

Abstract
Iodine may have an inhibitory and, in some circumstances, a stimulatory effect on thyroid follicular cell growth. Exogenous iodine deficiency causes the growth of endemic goitres and it has been claimed that low intrathyroidal iodine stores stimulate growth. On the other hand, the role of iodine, if any, in regulating the growth of human nodular goitres exposed to an ample supply of iodine has not been studied systematically. Very few data on intrathyroidal iodine concentration in this type of goitre are available.
In the present work we have investigated total iodine content in 24 samples from 11 clinically and histomorphologically well-defined fast and autonomously growing human nodular goitres from a non-endemic area. Iodine was fractionated into thyroglobulin-iodine and non-thyroglobulin-iodine. The regional distribution of intrathyroidal iodo-compounds was also assessed in three goitres.
Total iodine concentration, as well as its sub-fractions, i.e. thyroglobulin-iodine and non-thyroglobulin-iodine, were significantly lower than in normal thyroids. Furthermore, there was large inter- and intraindividual heterogeneity of all iodo-compounds as well as of thyroglobulin. Total iodine concentration varied by a factor of almost 40 between different goitre samples and by a factor of 20 between samples taken from the same goitre. Total non-thyroglobulin-iodine, the only fraction comprising possible cell growth-regulating iodocompounds, varied by a factor of >60 between different goitres and by a factor of >6 between different samples of the same goitre.
The low iodine concentration in all our goitre samples did not differ from values reported in the literature for endemic iodine-deficient goitres. Since all goitres studied here were actively growing while exposed to an ample supply of iodine, iodine shortage cannot be a primary and causal factor for the growth of this type of sporadic goitre. Rather, the low concentration and the large inter- and intraindividual heterogeneity of all iodocompounds appear to be secondary incidental events well explained by the recently developed concept of autonomous thyroid growth.
Journal of Endocrinology (1994) 140, 155–164
Glucagon binding to hepatocytes isolated from two teleost fishes, the American eel and the brown bullhead
Authors: Navarro I , Moon T W 
Published: December 2008

Abstract
We have characterized the specific binding of glucagon in hepatocytes isolated from two teleost species, the American eel (Anguilla rostrata) and the brown bullhead (Ictalurus nebulosus). Specific glucagon binding was 9·3 and 10·7% in bullhead and eel hepatocytes respectively, after a 2-h incubation at 12 °C. Curvilinear Scatchard plots suggest the presence of two classes of binding sites with apparent dissociation constants (Kd) of 1·97 nm (high affinity) and 17·3 nm (low affinity) for bullhead and 2·68 and 22·9 nm for eel cells. The number of high-affinity binding sites per cell was significantly higher in the eel (10 413) than in the bullhead (3811). The number of high-affinity insulin-binding sites was approximately two times higher than that for glucagon in bullheads and the opposite in the eel hepatocytes. In competition experiments, insulin did not displace 125I-labelled glucagon binding in the hepatocytes of either species, while glucagon-like peptide-1(7–37) (GLP-1) displaced glucagon but only at high concentrations, suggesting separate glucagon- and GLP-1-binding sites. The rate of dissociation of hepatocyte-bound 125I-labelled glucagon was similar for both species. Preincubation of hepatocytes in 100 nm glucagon decreased the number of high-affinity glucagon-binding sites by approximately 55% in both species, while the Kd values remained unchanged. Glucagon bound to the cell surface is internalized by fish hepatocytes. These properties indicate that the glucagon binding to hepatocytes of these two teleost species is similar to that reported for mammalian hepatocytes.
Journal of Endocrinology (1994) 140, 217–227
Inhibition of progesterone receptor function results in loss of basic fibroblast growth factor expression and stromal cell proliferation during uterine remodelling in the pregnant rat
Authors: Rider V , Psychoyos A 
Published: December 2008

Abstract
Recent studies suggest that hormonal control of uterine cell proliferation may be moderated by polypeptide growth factors. It remains to be determined, however, whether growth factors cause or are the consequence of hormone action. Basic fibroblast growth factor (bFGF) has been shown to influence cell proliferation and differentiation of a variety of mesoderm-derived cells. To elucidate the regulatory mechanisms controlling stromal cell proliferation and differentiation required for embryo implantation further, immunohistochemical localization of the progesterone receptor and bFGF have been studied. The cell-specific distribution of these proteins was determined in the rat uterus during early pregnancy and after injection of the progesterone receptor antagonist mifepristone (RU 486) at days 1 and 2 post coitum (p.c.) to block implantation. Cell division was restricted to luminal and glandular epithelial cells in pregnant and RU 486-treated rats at day 3 p.c. At day 4 of pregnancy, cell proliferation switched from the epithelia to the stroma in pregnant rats, but after RU 486 treatment division of stromal cells was inhibited significantly (P < 0·05). Progesterone receptor distribution was altered and bFGF was absent in RU 486-blocked stromal cells. Expression of bFGF in luminal and glandular epithelial cells, however, was insensitive to the effects of progesterone receptor antagonism. bFGF content was stimulated in the luminal epithelium and in decidual cells by the implanting embryo. These results indicate that repression of progesterone receptor function in early pregnancy results in a cell-specific loss of bFGF from stromal cells and inhibition of their proliferation. The results further suggest that the regulation of endometrial cell bFGF content is modulated at the site of implantation by the embryo.
Journal of Endocrinology (1994) 140, 239–249
Insulin-like growth factor-binding protein-1 is correlated with low density lipoprotein cholesterol in normal subjects
Authors: Hopkins K D , Lehmann E D , Parker J R , Gosling R G 
Published: December 2008

Abstract
Insulin-like growth factor-I (IGF-I) has been inversely associated with low-density lipoprotein (LDL) cholesterol in normal women with slightly elevated cholesterol levels and hypothyroid women. More than 95% of IGF-I circulates bound to binding proteins (IGFBPs); of these IGFBP-1 is of particular interest as it is inversely regulated by insulin and is thought to inhibit the action of IGF-I and IGF-II. We examined the relationship between IGFBP-1 and LDL cholesterol in 41 healthy adult subjects.
LDL cholesterol correlated with the body mass index (r=0·40, P<0·01), sex (r=0·51, P<0·001) and IGFBP-1 levels (r=0·36, P<0·02). LDL cholesterol did not correlate with age (r=0·25, P=not significant) or IGF-I (r=0·06, P=not significant). Upon multivariate regression analysis, sex, body mass index and IGFBP-1 were all independent predictors of LDL cholesterol (all P<0·05).
Elevated IGFBP-1 levels have been associated with an inhibition of serum IGF-I bioactivity in children with insulin-dependent diabetes. IGFBP-1 also appears to inhibit IGF-I hexose-stimulated uptake. IGFBP-1 may also be inhibiting the effect of IGFs on the cellular metabolism of LDL cholesterol.
Journal of Endocrinology (1994) 140, 521–524
ACTH STIMULATES MELANOGENESIS IN CULTURED HUMAN MELANOCYTES
Authors: Hunt G. , Todd C. , Kyne S. , Thody A.J. 
Published: December 2008

ABSTRACT
While ACTH is known to induce skin pigmentation in man, its effects on cultured human melanocytes have not been investigated. Using a culture system free of artificial mitogens, we report for the first time that ACTH stimulates melanogenesis in cultured human melanocytes. While ACTH, α-MSH and the synthetic α-MSH analogue Nle4DPhe7α-MSH all stimulate the activity of tyrosinase, the rate limiting enzyme in melanogenesis, and all produce a 50% increase in the melanin content of the cells at a concentration of 10−8-10−7 mol/l, the shapes of the dose response curves differ: those for the MSH peptides are sigmoidal while those for ACTH are biphasic. In addition, human melanocytes are able to respond to concentrations of ACTH comparable with physiological plasma levels. We suggest that ACTH may be relatively more important than α-MSH as a pigmentary hormone in man and could have a physiological role in skin pigmentation.
Periovulatory LHRH, LH and FSH secretion in cyclic rats treated with RU486: effects of exogenous LHRH and LHRH antagonist on LH and FSH secretion at early oestrus
Authors: Sánchez-Criado J E , Hernandez G , Bellido C , Gonzalez D , Tébar M , Diaz-Cruz M A , Alonso R 
Published: December 2008

Abstract
The antiprogesterone RU486 injected on the morning of pro-oestrus blunts the preovulatory secretion of LH and FSH and abolishes the secondary secretion of FSH during oestrus without affecting ovulation in the rat. To ascertain whether the secretion of LHRH is involved in these effects, we studied the effects of RU486 (4 mg/0·2 ml oil), given s.c. at 0800 h on pro-oestrus, on LHRH secretion into the pituitary stalk blood vessels and on peripheral plasma concentrations of LH and FSH at 1800 h on pro-oestrus and 0200 h on oestrus. Furthermore, we determined the effects of an s.c. injection of 1 mg of an LHRH antagonist (LHRH-A; ORG30276) at 2000 h on pro-oestrus and those of an i.p. injection of 100 ng LHRH (Peninsula 7201) at 0100 h on oestrus on serum concentrations of LH, FSH and oestradiol at 0200 h on oestrus in oil- and RU486-treated rats.
RU486 decreased LHRH secretion at 1800 h on prooestrus while this was increased at 0200 h on oestrus. While the reduction of preovulatory LHRH secretion in RU486-treated rats coincided with a reduction in both LH and FSH surges during the evening of pro-oestrus, the increased LHRH secretion during the early hours of oestrus was only accompanied by an increased concentration of LH. An injection of LHRH stimulated, while that of LHRH-A inhibited serum concentrations of LH at 0200 h on oestrus in both oil- and RU486-treated rats. An injection of LHRH-A had no effect on FSH concentration at 0200 h on oestrus in either oil- or RU486-treated rats. On the contrary, exogenous LHRH increased FSH concentration at 0200 h on oestrus only in oil-treated rats.
The results indicate that, in the rat, progesterone secretion during the afternoon and evening of pro-oestrus enhances preovulatory LHRH and suppresses LHRH release during early oestrus into the pituitary stalk blood vessels on the afternoon of pro-oestrus and during early oestrus respectively. While the secretion of LH during early oestrus is blunted by progesterone and entirely coupled to LHRH secretion, the secondary secretion of FSH during oestrus is not dependent on endogenous LHRH and at the same time is completely dependent on the actions (direct and/or indirect) of progesterone.
Journal of Endocrinology (1994) 141, 7–14
Production of anti-idiotypic antibodies resembling bovine somatotrophin by active immunization of lactating cows
Authors: Schalla C L , Roberge S , Wilkie B N , McBride B W , Walton J S 
Published: December 2008

Abstract
Anti-idiotypic antibodies produced in lactating cows by immunization with rabbit antibodies raised against bovine somatotrophin (bST) were evaluated for bST-like immunoactive and biological activities. Twenty New Zealand White rabbits were immunized against bST. Serum was purified using protein A–Sepharose CL-4B and bST–Sepharose 4B affinity chromatography to yield specific anti-bST immunoglobulin G (IgG). Twenty-four lactating cows were allocated to a randomized complete block design and were immunized with either: (1) rabbit anti-bST (n=12) or (2) non-specific rabbit IgG (n=12, control). Cows were immunized starting at day 68 of lactation with 800 μg antigen emulsified with Freund's complete adjuvant and 1 mg Quil A administered by i.m. injections. Repeated immunizations of 800 μg antigen in Freund's incomplete adjuvant and 1 mg Quil A followed after 3 weeks and then every 5 weeks throughout lactation. Serum samples were collected twice weekly and were analysed for anti-rabbit IgG titre and immunoactive bST concentration by radioimmunoassay. All cows developed antibodies against rabbit IgG by the second and third immunizations. With rising titres, immunoactive bST concentrations increased in cows treated with anti-bST following each of the six repeated immunizations to 4·7±3·3, 10·0±4·2, 12·0±4·8, 17·3±6·7, 24·0±10·0 and 36·3±20·4 ng/ml (mean±s.e.m.) compared with controls (0·81±0·09 ng/ml, overall mean±s.e.m.). To assess the biological activity of these bST anti-idiotypic antibodies, milk yield and serum insulin-like growth factor-I (IGF-I) concentrations were analysed in all cows and a subset of six cows per treatment respectively. Milk production and IGF-I concentrations were unaffected by anti-bST immunization.
Journal of Endocrinology (1994) 141, 203–208