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Biomedical subjects

C Kordon

Publications and source records attributed to C Kordon.

At least 163 records · Page 9Linked to original sources
PubMed1980

Kinetic characteristics of LH and FSH responses to LHRH in incubated pituitaries from ovariectomized or ovariectomized, estrogen-implanted rats.

Incubated pituitary halves from ovariectomized, estrogen-implanted female rats were shown to be much more sensitive to LHRH than pituitaries from castrated, nontreated animals. LHRH in a concentration of 1,885 pg/ml increased the release of LH and FSH from 7.3 +/- 0.9 and 0.91 +/- 0.13 ng/h/hemipituitary respectively to 21.4 +/- 1.9 and 1.97 +/- 0.18 ng/h in animals implanted with the steroid. In contrast, 5,000 pg/ml of LHRH increased LH secretion from 3.4 +/- 0.3 to 8.4 +/- 0.4 ng/h in ovariectomized, nontreated animals. In pituitaries from both steroid and nontreated animals a highly significant dose response for LH and FSH secretion to the actual concentration of LHRH measured in each incubation tube by radioimmunoassay was observed. When expressed as percent of the corresponding control release, maximal stimulation of LH and FSH was comparable. Pituitaries from implanted animals provided a very sensitive bioassay for LHRH, in which amounts of the peptide lower than 100 pg/ml were detected. The apparent responsiveness to LHRH of pituitaries from estradiol-treated rats was found to be over 20 times greater than that of pituitaries from nontreated castrates.

Animals↗
PubMed1980

Temporal relationships between the circadian rhythmicity in plasma levels of pituitary hormones and in hypothalamic concentrations of releasing factors.

Ovariectomized female rats were implanted with estradiol containing silastic implants to induce constant circulating levels of the steroid, and sacrificed every 2 h in order to determine neuroendocrine rhythms. Under these conditions, we observed very marked circadian fluctuations in the hypothalamic concentrations of corticotropin-releasing factor (CRF), luteinizing hormone-releasing hormone (LHRH) and thyrotropin-releasing hormone (TRH), and in plasma levels of adrenocorticotropin (ACTH), corticosterone, luteinizing hormone (LH) and prolactin; the amplitude of the prolactin cycle was in particular much higher than in non-chronically estrogenized animals. The daily variation in CRF, ACTH and corticosterone showed significant rank correlations. Changes in hypothalamic content of LHRH and TRH were biphasic; the increase observed during the light period was abruptly interrupted by a depletion episode, coincident with the period of maximal LH and prolactin secretion, respectively. The initial phase of ACTH, LH and prolactin increments occurred between 11.00 and 15.00 h, and was relatively well synchronized. The steepest rise in ACTH and prolactin occurred at the same time, and preceded that of LH by a constant lag of about 2 h. After that initial period, secretion kinetics of the three hormones followed an independent pattern. The data suggest that increased secretion of several hormones results from activation of neural mechanisms occurring within a limited period of the 24-hour cycle.

Adrenalectomy↗
PubMed1980

Stimulation of in vitro prolactin release by vasoactive intestinal peptide.

VIP stimulated prolactin secretion from incubated rat hemipituitaries. Under the same conditions, the secretion of GH, LH, FSH was not affected. The stimulation of prolactin was dose-dependent, with an apparent affinity of VIP of 10.9 +/- 3.1 nM and a maximal stimulation of 57.7 +/- 4.2%. Secretin, a structurally related peptide, was also active at higher concentrations whereas another partial analogue, glucagon, was ineffective. The effect of VIP was not blocked by alpha-flupentixol, a potent dopaminergic antagonist, at concentrations which antagonized the dopamine inhibition of prolactin secretion. Stimulation by VIP and TRH was additive. Neither Met-enkephalin nor naloxone interfered with the response to VIP. It thus seems that specific VIP receptors are present on pituitary prolactin cells. VIP, present in the mediobasal hypothalamus and detected in the hypothalamo-hypophyseal portal blood therefore is a good candidate as a physiological PRF.

Animals↗
PubMed1980

Effect of vasoactive intestinal peptide (VIP) on the release of adenohypophyseal hormones from purified cells obtained by unit gravity sedimentation. Inhibition by dexamethasone of vip-induced prolactin release.

The effect of vasoactive intestinal peptide (VIP) on the release of prolactin (PRL), gonadotropins (LH and FSH), growth hormone (GH) and corticotropin (ACTH) was studied using purified rat anterior pituitary cells obtained by means of velocity sedimentation at unit gravity. VIP, at concentrations ranging from 10(-10) to 10(-7) M, stimulated PRL secretion in a dose-dependent manner with an ED50 of 2 nM and a maximal response of 530% of control values. In contrast, similar concentrations of VIP did not affect the release of either LH, FSH, GH or ACTH from the corresponding enriched cell populations. Addition of dexamethasone (10(-9) M) to both preincubation and incubation medium of PRL cells completely inhibited VIP-induced PRL release. The present results further support the hypothesis that VIP is of physiological importance in the control of PRL secretion and demonstrate that corticosteroids can modify the responsiveness of PRL cells to VIP.

Animals↗
PubMed1980

Effect of steroids on vasoactive intestinal peptide in discrete brain regions and peripheral tissues.

The effect of castration and adrenalectomy was studied on vasoactive intestinal peptide (VIP) concentrations in various brain and peripheral structures of male rats. Castration has no effect on any of the structures studied, whereas 4 weeks adrenalectomy (ADX) decreases VIP concentrations in the hippocampus and increases them in the adenohypophysis, two structures known to contain large amounts of glucocorticoid receptors. Corticosterone administration restores VIP levels to control values only in the dorsal hippocampus. In contrast, dexamethasone counteracts both the decrease and the increase of VIP concentrations obtained after ADX in the hippocampus and in the adenohypophysis respectively. The present results suggest that corticosteroids can be involved in the regulation of VIP actions both in the brain and in the adenohypophysis.

Adrenalectomy↗
PubMed1980

Differences in the kinetics of dopamine uptake in synaptosome preparations of the median eminence relative to other dopaminergically inervated brain regions.

A comparison of the kinetics of dopamine uptake was made in synaptosomal preparations of the median eminence, striatum and olfactory tubercle. Double reciprocal Lineweaver-Burk plots of the initial velocity versus the concentration of dopamine yielded a single straight line in all three areas. The Michaelis constant (Km) in the median eminence (1.8 +/- 0.9 X 10(-6) M) was significantly higher (p < 0.05) than in the striatum (4.2 +/- 0.8 X 10(-8) M) or olfactory tubercle (6.3 +/- 1.9 X 10(-8) M). Uptake in the median eminence appeared to be predominantly into dopaminergic terminals since preincubation with desipramine did not affect the maximum velocity (Vmax) of dopamine uptake. Observed uptake was predominantly due to transport across the neuronal membrane and not into storage granules, since reserpine only caused a small decrease in uptake. The low affinity of dopamine uptake in median eminence synaptosomes is consistent with the neurosecretory nature of these terminals, whereas, in the striatum and olfactory tubercle, high affinity reuptake is consistent with the role of dopamine as a neurotransmitter.

Animals↗
PubMed1980

Monoaminergic regulation of growth hormone in the rat.

The administration of gamma-hydroxybutyrate (GHB) induced a consistent secretory episode of growth hormone (GH) in the morning followed by basal levels of secretion of GH for several hours. The measurement of endogenous noradrenaline, dopamine and serotonin (5-HT) following infusion of GHB showed that dopamine concentrations were significantly increased in the striatum; at the level of the hypothalamus, however, no significant differences were observed between control and GHB-treated animals. The data reported in this study are consistent with the interpretation that the neurotransmitter regulation of GH release and the modulation of hypothalamic glucoreceptor systems are not fundamentally different in rodents and primates. Clonidine, and alpha-adrenergic agonist, enhanced the peak of GH observed in the morning and caused a rapid increment of GH during the period when it was normally at basal levels. Under the same experimental conditions, dopamine agonists, apomorphine and levodopa, had no effect on GH secretion. The inhibition of catecholamine synthesis by alpha-methyl-p-tyrosine blocked the secretory episode of GH following administration of GHB and after insulin hypoglycaemia whereas the GH rise induced by clonidine was unchanged. The inhibition of 5-HT synthesis by p-chlorophenylalanine also suppressed the secretory episode of GH seen in the morning and the release of GH induced by hypoglycaemia; both being partly restored in animals pretreated with 5-hydroxytryptamine.

Animals↗
PubMed1980

[Effect of neuropeptides on prolactin secretion by the adenohypophysis (author's transl)].

In order to identify prolactin regulating factors, the effect of various neuropeptides on prolactin secretion by the adenohypophysis has been tested. 1 degree Histidyl-proline-diketopiperazine (DKP), a major degradation product of TRH in hypothalamus and pituitary, inhibited prolactin secretion from incubated hemipituitaries (Fig. 1) with an apparent affinity of 0.5 nM. Histidyl-prolineamide and histidyl-proline, other degradation products of TRH, had no effect. TSH secretion was not affected under the same conditions. 2 degrees Vasoactive intestinal peptide (VIP) stimulated prolactin secretion in vitro in a dose dependent manner. The secretion of other adenohypophyseal hormones was not affected. This effect is not mediated by a dopaminergic mechanism, since it was not blocked by neuroleptics (Table I). 3 degrees Morphinomimetic peptides had no effect on prolactin secretion in vitro, but blocked the dopamine inhibition of prolactin secretion. The effect of metenkephalin and beta-endorphin was dose dependent and was blocked by naloxone (Fig. 2 and 3). Thse results indicate that specific receptors to various neuropeptides seem to be present on prolactin cells.

Animals↗
PubMed1979

Vasoactive intestinal peptide inhibits release of somatostatin from hypothalamus in vitro.

The effect of vasoactive intestinal peptide (VIP) was studied on the release of somatostatin (SRIF) from slices of several regions of the rat brain in vitro. VIP induced a dose-dependent inhibition of SRIF release from mediobasal hypothalamic slices but did not interfere with SRIF release from preoptic area, amygdala or cortex. VIP inhibition had an apparent affinity: Kd = 6.8 +/- 3.9 x 10(-11) M. Secretin had a similar effect but at 600-fold higher concentrations (Kd secretin = 4.2 +/- 0.6 x 10(-8) M). Gucagon was ineffective in concentrations ranging from 10(-10) M to 10(-7) M. The data are consistent with a role of VIP in the hypothalamic control of growth hormone secretion.

Animals↗
PubMed1979

Subcellular distribution of brain peptidases degrading luteinizing hormone releasing hormone (LHRH) and thyrotropin releasing hormone (TRH).

The luteinizing hormone and thyrotropin-releasing hormones have been shown to be mostly concentrated in the nerve endings of the median eminence. In contrast, the peptidases responsible for their degradation present an ubiquitous localization and most of the reports have dealt with the total soluble activity. A detailed study of the subcellular distribution of these enzymes was thus performed in cerebral cortical and hypothalamic preparations of rat brain. The activity of a soluble marker, lactic dehydrogenase, was also measured to control for possible contaminants. The results showed that only 10% of peptidase activity was present in the nerve ending preparation. Evidence is provided for a non-neglible membrane-bound enzymatic component responsible for TRH degradation at the synaptosomal level of both cortex and hypothalamus.

Animals↗
PubMed1979

Subcellular distribution of corticotropin-releasing factor in the medio-basal hypothalamus of the rat.

Subcellular fractionation of the mediobasal hypothalamus (MBH) and frontal cerebral cortex was performed by differential and discontinuous sucrose gradient centrifugation. Corticotropin-releasing factor (CRF) activity of the different fractions was evaluated by bioassay. Significant CRF activity was found in acidic extracts of the MBH but not of the cerebral cortex. About 80% of the MBH effect on adrenocorticotropic hormone release was recovered in the crude mitochondrial pellet (P2) which contains synaptosomes. After further fractionation, distribution of CRF activity paralleled that of lactate dehydrogenase activity, a marker of the soluble cytoplasm. It is concluded that most CRF in the MBH is located in nerve endings as already shown for several other neurohormones.

Animals↗
PubMed1979

Effect of neurotransmitters on the in vitro release of immunoreactive thyrotropin-releasing hormone from rat mediobasal hypothalamus.

The in vitro release of TRH from hypothalamic fragments or purified nerve endings (synaptosomes) has been evaluated after incubation for 10 min in the presence of various concentrations of K+ or neurotransmitters. Release of the hormone from fragments but not from synaptosomes was enhanced in the presence of 56 mM K+ in a Ca++ -dependent manner. Neurotransmitter effects were thus tested on the fragments. Addition of histamine (10 (-7)-10(-5) M) induced a significant increase over the basal release of TRH. A comparable effect was obtained with dimaprit (10(-5) M), a highly specific agonist of histamine H2 receptors; conversely, the response to histamine was blocked by the addition of a H2 (metiamide; 10(-6) M) but not of a H1 (mepyramine; 10(-6) M) antagonist to the incubation medium. Dopamine (10(-7) M) slightly inhibited the release of TRH, but antagonists of dopamine receptors (10(-7)-10(-6) M fluphenazine or 10(-6) M alpha-flupentixol) exhibited an inhibitory effect by themselves, so that specific receptors involved in mediating dopamine actions could not be further characterized. In contrast, noradrenalin, serotonin gamma-aminobutyric acid and acetylcholine (tested at concentration of 10(-7) M) did not alter the basal release of the tripeptide.

Amino Acids↗