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H Vaudry

Publications and source records attributed to H Vaudry.

At least 559 records · Page 31Linked to original sources

Identification of a second category of alpha-melanocyte-stimulating hormone (alpha-MSH) neurons in the rat hypothalamus.

An immunocytochemical localization of alpha-melanocyte-stimulating hormone (alpha-MSH) as well as ACTH and a fragment (16K) of the common precursor of ACTH and beta-lipotropin (beta-LPH) was performed in rat brain. Two different groups of neuronal cell bodies showing alpha-MSH-like immunoreactivity (alpha-MSH-LI) were observed in the hypothalamus. One group of neurons located in the arcuate nucleus was shown to contain not only alpha-MSH-LI, but also ACTH and the 16K fragment. A second category of alpha-MSH-LI-containing neurons was characterized by the complete absence of staining for ACTH and 16K fragment. These neurons were mainly located in the dorsal-lateral portion of the hypothalamus. Immunoelectron microscopy showed that immunostaining for alpha-MSH was restricted to dense core vesicles in the positive perikarya. Nerve fibers staining for alpha-MSH (but not for ACTH and 16K fragment) were also observed outside the ACTH-beta-LPH pathway, especially in the cortex, caudate-putamen nucleus and hippocampus. These findings strongly suggest the presence of two different neuronal systems reacting with antibodies to alpha-MSH.

Adrenocorticotropic Hormone↗

Immunohistochemical localization of gamma-endorphin in the rat pituitary gland and hypothalamus.

To gain more information about cells and organelles involved in the secretion of gamma-endorphin in the rat pituitary gland, an immunohistochemical localization of this peptide was conducted at both light and electron microscopic levels. Using an antiserum to gamma-endorphin which shows little cross-reactivity with beta-lipotropin (beta-LPH) and beta-endorphin, it has been demonstrated that gamm-endorphin is present in all cells of the intermediate lobe and the corticotropic cells of the anterior lobe. At the electron microscopic level, staining for gamma-endorphin was restricted to the secretory granules which also contain ACTH and beta-LPH, suggesting that all of these peptides are released concomitantly during exocytosis. In the hypothalamus, immunostaining possibly related to both gamma- and beta-endorphin but not to beta-LPH was also observed in nerve fibers and not in cell bodies.

Animals↗

beta-Endorphin and met-enkephalins: their distribution, modulation by estrogens and haloperidol, and role in neuroendocrine control.

A single dose of 0.5 micrograms beta-endorphin injected intraventricularly in unanesthetized male rats bearing chronic intraventricular and intrajugular cannulas led to a sevenfold stimulation of plasma prolactin (PRL) levels 10 to 20 min after injection of the peptide, while a dose of 2 micrograms of beta-endorphin led to a comparable stimulation of plasma growth hormone (GH) concentration. Met-Enkephalin was much less potent than beta-endorphin in stimulating PRL and GH release. Naloxone, a specific opiate antagonist, completely blocked the stimulation of GH and PRL release at the doses of 0.5 and 12.5 mg/kg, respectively. beta-Endorphin and Met-enkephalin from 41 discrete brain nuclei were measured by radioimmunoassay (RIA). beta-Endorphin was found in the hypothalamus medial preoptic nucleus, nucleus interstitialis striae terminalis (NIST), nucleus medialis thalami, and periaqueductal gray. Met-Enkephalin was found predominantly in the globus pallidus, NIST, medial preoptic nucleus, nucleus amygdaloideus centralis, and nucleus lateralis hypothalami. Treatment with both estrogens and haloperidol led to differential effects on Met-enkephalin content in various brain nuclei. Estrogen treatment increased Met-enkephalin levels in globus pallidus, NIST, medial and lateral preoptic nuclei, and periaqueductal gray, while a decrease of the Met-enkephalin content in the nucleus amygdaloideus centralis was found. Haloperidol treatment led to a stimulatory effect in striatum, medial and lateral preoptic nuclei, and interpeduncular nucleus.

Animals↗

Comparative effects of canrenoate-K and prorenoate-K upon aldosterone biosynthesis in perifused frog interrenal glands.

To investigate the possible direct effect of two aldosterone antagonists (Canrenoate-K and Prorenoate-K) upon mineralocorticoid biosynthesis a perifusion system technique has been developed. Frog interrenal tissue was selected for its ability to secrete huge amounts of aldosterone (twice as much as corticosterone in resting conditions). Throughout the experiment, secretion of aldosterone was measured every ten minutes by means of a sensitive and highly specific radioimmunoassay method. Increasing concentrations of both Canrenoate-K and Prorenoate-K (ranging from 10(-4)M to 10(-3)M) caused a dose-related inhibition of aldosterone output. At a dose of 3.16 x 10(-4)M, Prorenoate-K appeared to be somewhat more potent (57.8% inhibition) than Canrenoate-K (47.8% inhibition). Infusion of both Canrenoate-K and Prorenoate-K at a dose of 5 x 10(-4)M during 1 or 2 hours induced a similar sharp decrease in mineralocorticoid secretion. Thus, it appears that Canrenoate-K and Prorenoate-K beside their well known effects at renal tubular receptor sites do also inhibit aldosterone biosynthesis. These results indicate that in vivo administration of aldosterone antagonists may first involve a transient decrease in aldosterone secretion. Furthermore, they suggest that mineralocorticoid biosynthesis might be regulated by a short loop feedback mechanism.

Adrenal Glands↗

Biological and radioimmunological evidence for melanocyte stimulating hormones (MSH) of extrapituitary origin in the rat brain.

The possible existence of extrapituitary melanocyte stimulating hormone (MSH) in various regions of the rat brain has been studied in intact and hypophysectomized rats. Using a sensitive and specific radioimmunoassay (RIA), alphaMSH has been found in a number of brain regions in intact rats. The standard curves of synthetic alphaMSH and the dilution curves for pars intermedia nervosa (PIN), pars distalis (PD), hypothalamus and thalamus extracts were strictly parallel. The alphaMSH concentrations were measured in PIN (6,225 +/- 962 ng/mg wet tissue); PD (12.5 +/- 1.41 ng/mg); pineal (380 +/- 29 ng/g wet tissue); hypothalamus (645 +/- 161 ng/g) and thalamus (33.3 +/- 5.26 ng/g). In rats hypophysectomized for 1 or 2 months, the highest concentrations of immunoreactive alphaMSH were found in pineal (353 +/- 140 ng/g wet tissue), hypothalamus (85.8 +/- 14.1 ng/g) and thalamus (39.8 +/- 13.9 ng/g). Hypophysectomy significantly reduced hypothalamic MSH content and concentration but did not alter MSH concentration in pineal and thalamus. From these results, we conclude that hypothalamic alphaMSH is, in part, of hypophyseal origin while pineal and thalamus alphaMSH does not originate from the pituitary. After Sephadex G-25 gel filtration, synthetic alphaMSH and PIN extracts showed a single peak of both bioactive and immunoreactive alphaMSH. In the same conditions, extracts from the 5 brain regions studied in hypophysectomized rats chromatographed as a single peak of immunoreactive MSH but as 2 peaks of apparent bioactive MSH, 1 concident with synthetic alphaMSH and the other far after the salt volume. We conclude that alphaMSH is found in a number of brain areas and its presence after hypophysectomy would indicate synthesis within the central nervous system.

Animals↗

[Control of pituitary secretion of melanotropin in an anuran amphibian by thyrotropin releasing factor (TRH). Study in vitro].

Intermediate lobes from Rana esculenta pituitary glands were continuously superfused for 7 hrs at 28 degrees C with amphibian culture medium. alpha-MSH release was measured by use of a sensitive double antibody radio-immunoassay system. alpha-MSH secretion was inhibited by low temperatures. A large increase in alpha-MSH release was observed when Thyrotropin Releasing Hormone (TRH) at doses ranging from 10(-9) to 10(-7) molar was added to the superfusion medium. Since large amounts of TRH are to be found in the hypothalamus of amphibians but have no effect over pituitary TSH secretion, the action of TRH over alpha-MSH release may have a physiological significance.

Animals↗

[Competitive protein-binding radioassay of corticosterone in the plasma of the frog, Rana esculenta L. (author's transl)].

1. Plasma corticosterone levels were measured in the plasma of the edible frog, Rana esculenta, by a competitive protein-binding radioassay method using baboon plasma as CBG source. 2. This technique was sensitive enough to make the assessment of corticosterone levels in 50 microliter plasma samples possible. The assay sensitivity threshold reached 0.5 ng per tube and the corticosterone rate assessment was correct between 0 and 5 ng. The specificity was tested, using 12 different steroids (fig. 2) : baboon CBG had very slight avidity for aldosterone, the second circulating steroid in frog plasma. 3. Using this technique, we have shown that plasma corticosterone underwent seasonal variations. Plasma corticosterone levels, in animals captured in nature during February and June, were 1.51 +/- 0.06 microgram/100 ml (n = 60) and 2.76 +/- 0.14 microgram/100 ml (n = 36), respectively, as appeared in table III. 4. It appeared that the interrenal gland of the frog was not totally dependent on pituitary ACTH, since total hypophysectomy reduced, but did not suppress, corticosterone secretion (table III).

Animals↗