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F J Tilders

Publications and source records attributed to F J Tilders.

At least 127 records · Page 7Linked to original sources
PubMed1981

Hypothalamic deafferentation in the rat appears to discriminate between the anterior lobe and intermediate lobe response to stress.

Anterolateral deafferentation of the mediobasal hypothalamus prevented the increase of the plasma corticosterone concentration induced by ether, histamine and electric footshock. Hypothalamus deafferentation also prevented the ether stress-induced increase of the plasma levels of ACTH and beta-endorphin immunoreactivity (ACTHi, beta-ENDi). Infusion of isoproterenol evoked an increase of the plasma levels of corticosterone, ACTHi, beta-ENDi and alpha-MSH immunoreactivity (alpha-MSHi) in sham-operated rats. In rats with a deafferented hypothalamus, the responses of plasma corticosterone and ACTHi to isoproterenol were blocked but the responses of plasma beta-ENDi and alpha-MSHi remained intact. We conclude that circulating beta-ENDi after exposure to ether is of anterior lobe origin while circulating beta-ENDi after infusion of isoproterenol is of intermediate lobe origin.

Adrenocorticotropic Hormone↗
PubMed1981

Epinephrine as a potent releaser of immunoreactive beta-endorphin in rats.

The intravenous infusion of catecholamines to rats induced a dose dependent increase of immunoreactive beta-endorphin (beta-Endi) in plasma. The ED50 values of 1-epinephrine and 1-isoproterenol were 110 and 100 ng/kg X min respectively. 1-Propranolol, but not d-propranolol prevented the effect of 1-epinephrine. Infusion of 100 ng/kg X min of 1-epinephrine increased plasma epinephrine to 11 pmol/ml, a concentration that can occur during stress. We conclude that circulating catecholamines can stimulate beta-Endi secretion via a beta-adrenergic receptor mechanism and may play a role in the response of beta-Endi to stress.

Animals↗
PubMed1981

Release of beta-lipotropin and beta-endorphin from rat hypothalami in vitro.

Hypothalamic tissue extracts of rats were chromatographed and beta-endorphin immunoreactivity (beta-Endi) was measured. The two major peaks of beta-Endi co-eluted with beta-lipotropin (beta-LPH) and beta-End respectively. Hypophysectomy caused a local decrease of beta-LPH and beta-End concentrations in the mediobasal hypothalamus. During superfusion of hypothalamic tissue blocks in vitro, membrane depolarization by electric stimulation or 45 mM k+ induced a Ca2+-dependent release of both beta-LPH and beta-End.

Animals↗
PubMed1981

Distribution, subcellular localization and identity of immunoreactive alpha-melanotropin in the pituitary gland and brain.

In homogenates of adult human or rat hypothalamic tissue, immunoreactive alpha-MSH (alpha-MSHi) is concentrated in synaptosomes, suggesting that it is localized in neurons. This conclusion is supported by immunohistochemical results on the localization of alpha-MSHi in the brain. The function of alpha-MSHi in the hypothalamus is undefined but the amount of alpha-MSH in this tissue increases in young rats and decreases in old rats. There is little alpha-MSHi in pituitary glands from human abortuses before the 15th gestational week. Thereafter the amount of alpha-MSHi in the anterior and neurointermediate lobes increases appreciably. When acetic acid extracts of each lobe were analysed by high-pressure liquid chromatography the alpha-MSHi in extracts of the anterior lobe had a retention time equal to that of desacetyl alpha-MSH; little if any alpha-MSHi had a retention time identical to that of desacetyl alpha-MSH; alpha-MSH, if present in these extracts, appeared to be a minor component. A similar analysis of extracts of adult human hypothalamic tissue yielded results suggesting that the alpha-MSHi in this tissue is also attributable largely to desacetyl alpha-MSH.

Adult↗
PubMed1981

Characterization of immunoreactive alpha-melanocyte stimulating hormone (alpha-MSHi) in human brain tissue.

Adult human hypothalamic tissue was analyzed for the presence of products generated by post-cleavage processing of ACTH 1-13. The displacement curve generated by immunoreactive alpha-melanocyte stimulating hormone (alpha-MSHi) in extracts (5 M acetic acid or acidified ethanol) of adult human hypothalamic tissue was parallel to the alpha-MSH radioimmunoassay standard curve, and alpha-MSHi eluted as a single peak on Sephadex G-10, G-25, and G-50 columns in a manner identical to that of synthetic alpha-MSH. The alpha-MSHi was clearly distinguishable in its mobility on Sephadex G-50 columns from such peptides as beta-MSH, luteinizing hormone releasing hormone, and ACTH. After high performance liquid chromatography of extracts of hypothalamic tissue from young as well as aged men and women, we found that the major peak of alpha-MSHi (75-95% of total alpha-MSHi) coeluted with desacetyl alpha-MSH (ACTH 1-13 amide) rather than alpha-MSH. We suggest that desacetyl alpha-MSH, rather than alpha-MSH, is the predominant alpha-MSHi in adult human brain tissue.

Adrenocorticotropic Hormone↗
PubMed1981

The major immunoreactive alpha-melanocyte-stimulating hormone (alpha MSH)-like substance found in human fetal pituitary tissue is not alpha MSH but may be desacetyl alpha MSH (adrenocorticotropin1-13NH2).

Pituitary glands were obtained from human abortuses during the second half of gestation. Acid extracts were made from the anterior and neurointermediate lobes, and alpha MSH immunoreactivity (alpha MSHi) was quantified by RIA. alpha MSHi was found in both lobes of the pituitary gland, with 20-80% of the total pituitary alpha MSHi being present in extracts of the anterior lobe. Anterior and neurointermediate lobe extracts subjected to gel filtration on Sephadex G-50 revealed one peak of alpha MSHi having an elution profile identical to those of alpha MSH and desacetyl alpha MSH (ACTH1-13NH2). To characterize further the alpha MSHi extracts were subjected to high pressure liquid chromatography. No alpha MSH could be identified in extracts of the anterior lobe, and most of the alpha MSHi had an elution profile identical to that of desacetyl alpha MSH. Although small amounts of alpha MSH might be present in the neurointermediate lobe, most of the alpha MSHi in this lobe coeluted with desacetyl alpha MSH. Since alpha MSH was not converted to desacetyl alpha MSH during the extraction and chromatographic procedures, we hypothesize that the predominant form of alpha MSH-like material in the human fetal pituitary gland may be desacetyl alpha MSH.

Adrenocorticotropic Hormone↗
PubMed1981

beta-Adrenergic stimulation of the release of ACTH- and LPH-related peptides from the pars intermedia of the rat pituitary gland.

The intermediate lobe of the rat pituitary gland produces a series of peptides related to ACTH and LPH. The spontaneous and isoproterenol-stimulated release of such peptides was studied during in vitro superfusion of rat neurointermediate lobes with Krebs-Ringer medium. Products released into the superfusion medium were quantified by direct measurement or after chromatography on Sephadex G-50. ACTH bioactivity was determined by use of adrenal cortical cell suspension assay. In addition, NH2-terminal ACTH, CO2H-terminal ACTH, alpha-MSH and beta-endorphin radioimmunoassays were used. The results show that 1. neurointermediate lobes of rats secret spontaneously various ACTH- and LPH-related peptides in amounts proportional to the amounts in which these peptides are found in extracts of the neurointermediate lobe; 2. the beta-adrenergic agonist, isoproterenol, stimulated the spontaneous release of various peptides, including alpha-MSH, ACTH, CLIP, glycosylated CLIP, and beta-endorphin-like peptides; 3. isoproterenol induced a dose-dependent (10(-9)-10(-7) M), parallel increase in the release of alpha-MSH and ACTH following similar time courses and showing identical EC50 values (about 10(-8)M). Although the spontaneous release of alpha-MSH and ACTH from rat neurointermediate lobes is not strictly coupled under the conditions used in this study, isoproterenol seems to affect the spontaneous release of these peptides to the same relative extent.

Adrenergic beta-Agonists↗
PubMed1980

A scanning microfluorimetric study on sympathetic nerve fibres: intraneuronal differences in noradrenaline turnover.

The quantitative aspects of formaldehyde induced fluorescence (FIF) of noradrenaline (NA) in sympathetic nerve fibres were studied in whole mount preparations of the iris of the rat. Both "static" and scanning microfluorimetric measurements showed a close linear relationship between the FIF intensity and the NA content after pharmacological treatment (alpha-methyl-p-tyrosine, amphetamine, guanethidine, nialamide). A histogram analysis method is described to study fluorescence changes in different parts of the nerve fibre histogram, in order to evaluate changes in different segments of the nerve fibres characterized by their fluorescence intensity. The method is illustrated by a study on NA turnover. The chemically determined halflife (T 1/2 of NA after alpha-methyl-p-tyrosine (4.3 h) was in close agreement with the T 1/2 estimated microfluorimetrically (4.2 h). However, pronounced differences were found in various parts of the nerve fibre histogram (3.7-6.3 h). We conclude that the turnover of NA is different in various segments of the sympathetic nerve fibres in the rat iris and that the most intensely fluorescent varicosities display the longest T 1/2 and the highest turnover rate of NA.

Adrenergic Fibers↗
PubMed1980

Microfluorimetric scanning of sympathetic nerve fibers: quantification of neuronal and extraneuronal fluorescence with the aid of histogram analysis.

A high resolution (0.5 micrometer), two-dimensional microfluorimetric scanning procedure was used to quantitate the formaldehyde-induced fluorescence of noradrenaline in the iris of the rat. Scanning of large areas (50 x 50 micrometer) in the sympathetic innervated dilator muscle revealed an overlap between measurements of nerve fibers and of background (smooth muscle). In order to discriminate between both populations, the scan data were converted into fluorescence histograms (256 fluorescence classes, and subjected to mathematical analysis. The characteristics of the background histogram were obtained from scans of iris preparations devoid of fluorescent nerve fibers (pretreatment of the donor rat with reserpine or sympathetic denervation). A curve-fitting program was applied on those fluorescence classes in the normal iris histogram that represent measurements on pure background and resulted in a full background histogram. After subtraction of this background histogram from the original histogram, a nerve fiber histogram was obtained. The validity of the algorithm was evaluated by scanning iris preparations with varying background intensities. The results showed that quantification of the nerve fiber fluorescence was independent of variation in the background.

Adrenergic Fibers↗
PubMed1980

The failure of L-prolyl-L-leucylglycinamide to inhibit the release of alpha-melanocyte-stimulating hormone in the rat.

We have studied the effect of L-prolyl-L-leucyglycinamide (PLG) on the release of melanocyte-stimulating hormone (MSH) from the rat pituitary gland both in vitro and in vivo. Superfusion of neurointermediate lobes with medium containing PLG or PLG-acetate (dose range 1-1000 ng/ml) did not affect the spontaneous release of MSH as determined by radioimmunoassay or by bioassay. Also during static incubations of rat hemipituitaries, PLG (6.6-50 ng/ml) was without effect on alpha-MSH release. Administration of PLG (1-250 ng iv) to intact male and female rats and rats being lesions in the medio-basal hypothalamus did not induce a fall in serum alpha-MSH levels. It is concluded that PLG does not affect the release of alpha-MSH from the rat intermediate lobe. It is unlikely therefore that PLG mediates the inhibitory influence of the CNS on MSH release.

Animals↗
PubMed1979

Identification of MSH release-inhibiting elements in the neurointermediate lobe of the rat.

Neurointermediate lobes of rats comprise elements which, when excited in vitro, bring about an inhibition of the release of melanocyte stimulating hormone (MSH). Superfusion of neurointermediate lobes of intact donor rats with medium containing 45 mM K+ induced a stimulation of the release of oxytocin, arginine-vasopressin and dopamine (DA) and inhibited the release of MSH. Fluorescence histochemical observations and the results of release studies indicate that electrothermic lesions in the mediobasal hypothalamus induced a more rapid degeneration of dopaminergic than of peptidergic terminals in the neurointermediate lobe. Dopaminergic nerve terminals and the stimulated release of DA had vanished completely on the second day after these lesions, which coincided with the disappearance of K+-induced inhibition of MSH release. Frontal hypothalamic deafferentations resulted in disappearance of peptidergic nerve terminals as evidenced by the development of diabetes insipidus and the strong decline of depolarization-induced release of oxytocin and vasopressin from neurointermediate lobes in vitro. In contrast, the dopaminergic plexus was left intact, as was the K+-induced stimulation of DA release and inhibition of MSH release. We conclude that the K+-induced inhibition of MSH release is mediated by DA rather than by neuropeptides from terminals in the neurointermediate lobe. The results are in agreement with the proposed MSH release-inhibiting role of the dopaminergic tuberoinfundibular neurones.

Afferent Pathways↗
PubMed1979

On the presence of extraneuronal catecholamine in the iris of the rat: a scanning microfluorimetric study.

Formaldehyde-induced fluorescence (FIF) of noradrenalin (NA) was studied in histochemical preparations of the rat iris. With the aid of a two-dimensional microfluorimetric scanning method, quantitative information was obtained from neuronal and non-neuronal elements selectively. Spectral analysis and fluorimetric studies showed the existence of extraneuronal NA in the iris of untreated rats. Surgical and pharmacological (reserpine, amphetamine, imipramine, nialamide) manipulation of sympathetic neurotransmission-induced changes in extraneuronal fluorescence, which did not parallel changes in fluorescence of neuronal elements. A positive relationship was found between changes in extraneuronal fluorescence and the postsynaptic effect (pupil diameter). We hypothesize that extraneuronal catecholamine (CA) fluorescence is a histochemical parameter for synaptic neurotransmission.

Animals↗
PubMed1979

The effect of hypothalamic lesions on immuno-reactive alpha-melanocyte stimulating hormone secretion in the rat.

We have examined the hypothesis that MSH secretion in the rat is under a tonic inhibitory control by the central nervous system. Electrothermic lesions were made in the medio-basal hypothalamus (m.b.h.) which destroyed the hypothalamo-hypophyseal connexions. Plasma and pituitary alpha-MSH wwere measured using a sensitive and specific radioimmunoassay technique. Pituitary alpha-MSH content decreased to 17% of control levels 24 hr after the lesion and returned to normal by 7 days. Plasma alpha-MSH was maximally elevated 15 min after the lesion, and returned to normal by 2 hr. No further change over control levels was found for the remainder of the experiment (98 days). The similarity of the plasma alpha-MSH response after m.b.h. lesions to that found previously after administration of long acting dopamine receptor blocking drugs suggests that these lesions may interrupt impulse flow in dopaminergic tubero hypophyseal neurones which are thought to be important in the inhibitory control of MSH secretion in the rat. From our present results it seems that the rat pituitary, unlike that of lower vertebrates, is able to re-establish basal MSH secretion very quickly after disconnexion from central control.

Animals↗