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Biomedical subjects

F J Tilders

Publications and source records attributed to F J Tilders.

At least 145 records · Page 8Linked to original sources
PubMed1978

Effects of hypothalamic lesions and drugs interfering with dopaminergic transmission on pituitary MSH content of rats.

The physiological significance of the dopaminergic innervation of the pars intermedia was studied in rats. Electrothermic lesions were made in the mediobasal hypothalamus in order to destroy all hypothalamo-hypophysial connections. Pituitary MSH content decreased to 25% of control values 8 h after lesioning. From the 1st day, however, pituitary MSH content gradually increased, reaching control levels after about 1 week. Haloperidol and pimozide (both neuroleptics) were used to block specifically dopamine (DA)-receptors. Single administration of these drugs induced a time and dose dependent reduction in pituitary MSH. A maximal decrease to about 60% was found 4-5 h after i.p. administration of 2.5 mg/kg haloperidol and 1.0 mg/kg pimozide. Apomorphine and 2-Br-alpha-ergocryptine (DA-receptor stimulating drugs), had no effect on pituitary MSH stores of intact rats, but completely prevented the lesion-induced fall in pituitary MSH content. The results show that DA-receptors located within the pituitary itself are involved in the control of MSH release indicating that the effect of hypothalamic lesions on pituitary MSH content is primarily caused by interruption of dopaminergic neurotransmission in the hypophysis. We conclude therefore that the dopaminergic arcuato-hypophysial neurones innervating the pars intermedia tonically inhibit the release of MSH in intact rats.

Animals↗
PubMed1978

Microfluorimetric scanning of sympathetic nerve fibers. An improved method to quantitate formaldehyde induced fluorescence of biogenic amines.

A two dimensional scanning procedure was developed for studying quantitative aspects of formaldehyde induced fluorescence (FIF) from noradrenaline containing nerve fibers. A computer (PDP 12) controlled scanning device was equipped with a cooled photomultiplier, a 0.5 micron scanning stage and a 0.5 micron measuring spot. Photodecomposition was reduced by a high scanspeed (100/sec) and a small excitation field. Digitized images were obtained with a high resolution. Data (10,000/scan) of large scan areas (2500 micron2) in the iris of the rat were transformed into fluorescence histograms, which allowed statistical evaluation. Visible changes induced in the histochemical preparation by administration of drugs (reserpine, L-Dopa) were reflected in characteristic changes in the histograms. A minor reduction in noradrenaline content, which was too small to be detected by visual observation of the microscopical image and by classical microfluorimetric methods, did evoke a significant change in the histograms. It is concluded that microfluorimetric scanning is a very sensitive technique for detecting changes of formaldehyde induced fluorescence from neuronal networks.

Adrenergic Fibers↗
PubMed1976

Stimulation of intra-uterine growth in rat by alpha-melanocyte-stimulating hormone.

We have studied whether endogenous alpha-MSH has a function in stimulating intra-uterine growth in the rat. The approach used was to determine whether or not this hormone is present during the intra-uterine growth spurt, and if binding of endogenous foetal alpha-MSH by antibodies would inhibit this growth. Antibodies against alpha-MSH or ACTH 1-24, either purified or non-purified, induced immunofluorescence in the intermediate lobe of adult male control rats. Using purified anti-alpha-MSH, fluorescence appeared in the foetal intermediate lobe on day 18 of pregnancy, the day that biologically active MSH was first seen. A negative correlation was observed between the pituitary MSH content and foetal body weight only on day 19 of pregnancy. Injection of purified anti-alpha-MSH induced a drop in foetal body weight, but no effect on placental weight was observed. Purified anti-acth 1-24 had no effect upon body weight but caused an increase in placental weight. These results support our previous findings and indicate that endogenous MSH has a function in the stimulation of foetal growth.

Adrenocorticotropic Hormone↗
PubMed1975

A diurnal rhythm in melanocyte-stimulating hormone content of the rat pituitary gland and its independence from the pineal gland.

Resting pituitary melanocyte-stimulating hormone (MSH) content was studied in adult rats kept under a controlled 14 h light-10 h dark regimen. A diurnal rhythm was found in pituitary MSH levels, showing peak values at 4.00-6.00 p.m., and low values during darkness and the beginning of the light period. The normally occurring fall in pituitary MSH content between 6.00 p.m. and midnight was also found in rats exposed to a prolonged photoperiod. Sympathetic denervation of the pineal gland by superior cervical ganglionectomy, as well as pinealectomy, did not block the rhythm in pituitary MSH, and had no effect on pituitary MSH content. In addition, melatonin administered i.v. did not affect pituitary MSH levels, either when MSH activity was tested on the Anolis skin in vitro, or when the in vivo assay with hypophysectomized frogs (Rana pipiens) was used. It was concluded that the diurnal rhythm in pituitary MSH content is not directly related to the light-dark cycle and is not controlled by pineal melatonin or any otherpineal factor.

Animals↗
PubMed1975

On the presence of a MSH-release inhibiting system in the rat neurointermediate lobe.

Rat neurointermediate lobes were superfused in vitro and showed a stable secretion rate of MSH after 30 min. MSH secretion from lobes of untreated rats was reversibly inhibited during superfusion with medium containing 45 mM K+. This inhibition could not be induced using lobes from median eminence lesioned or reserpinized rats. Superfusion with 45 mM K+ also induced release of dopamine from lobes preincubated with the labeled transmitter. It is concluded that the MSH-release inhibiting system present in the rat neurointermediate lobe may be identical to the dopaminergic arcuate-intermediate lobe system.

Animals↗
PubMed1975

Re-introduction and evaluation of an accurate, high capacity bioassay for melanocyte-stimulating hormone using the skin of Anolis carolinensis in vitro.

A simple and rapid assay for the quantitative determination of melanocyte-stimulating hormone (MSH) activity, using skin fragments of the lizard Anolis carolinensis in vitro, is described in detail. This assay, in which a quantal response (e.g. induction of a brownish-green colour) can be detected by visual observation, allows determination of MSH activity in up to 50 samples/day by one person, using the skin of one lizard. The mean dose found to induce this colour change was 0-15 ng synthetic alpha-MSH/ml (range 0-02-0-5 ng/ml). The assays shows high accuracy, reproducibility and specificity. Anterior and posterior lobe hormones as well as pituitary catecholamines do not interfere with the determination of pituitary MSH activitymthe method is compared with the assay using hypophysectomized frogs (Rana pipiens) in vivo. Determinations of MSH in pituitary extracts by both methods gave quantitatively similar results when determined with alpha-MSH as the reference substance. However, when beta-seryl MSH was used as a reference, the two assays gave different results for the MSH activity of the pituitary extractsmthis indicates that MSH from the rat pituitary gland has a biological activity similar to that of alpha-MSH rather than to that of beta-seryl MSH.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Quantification of formaldehyde induced fluorescence and its application in neurobiology.

The methods used for measurements of fluorescence intensity in histochemical preparation will be described. Under certain conditions, the FIF intensity of biological objects shows a linear relationship with the local monoamine concentration. Microfluorometry enables determination of changes in monoamine concentrations in cell bodies, terminal axons and extraneuronal structures. In certain neuronal systems, FIF intensity of cell bodies appears to be correlated with neuronal activity. FIF intensity measurements of terminal axons can provide information on turnover of monoamine in structures as small as individual varicosities. Finally, the significance of extraneuronal FIF intensity in relationship to neurotransmission will be discussed. This paper aims to show that determinations of FIF provide information on the functional activity of neuronal systems.

Animals↗
PubMedDate not supplied

Beta-adrenoceptor activation mediates stress-induced secretion of beta-endorphin-related peptides from intermediate but not anterior pituitary.

Recently, we reported that adrenaline can stimulate the secretion of immunoreactive beta-endorphin in the rat. This response is mediated by beta-adrenoceptors and requires circulating adrenaline concentrations which are known to occur during stress. We therefore studied whether catecholamines are implicated in the stress-induced secretion of immunoreactive beta-endorphin from the pituitary gland. We report here that in rat the beta-adrenoceptor antagonist (-)propranolol reduces or abolishes the rapid increase of immunoreactive beta-endorphin levels during some stress stimuli (footshock, passive avoidance, restraint) but not during others (ether, formalin, laparotomy). The propranolol-sensitive response is largely prevented by extirpation of the neurointermediate lobe of the pituitary gland but is unaffected by dexamethasone, which inhibits peptide secretion from the corticotroph cells of the anterior lobe. These results suggest that catecholamines activate the release of immunoreactive beta-endorphin from the intermediate lobe but not from the anterior lobe of the pituitary gland during certain stress conditions.

Animals↗
PubMedDate not supplied

Bacterial endotoxin induces fos immunoreactivity in primary afferent neurons of the vagus nerve.

Subdiaphragmatic vagotomy inhibits brain-mediated illness responses to peripherally administered bacterial endotoxin, including fever, hyperalgesia, sickness behavior, and activation of the hypothalamic-pituitary-adrenal axis. However, direct evidence implicating vagal afferents specifically in conveying information about peripheral immune activation to the brain is still lacking. This study assessed whether (1) endotoxin induces the expression of the functional activation marker Fos in the vagal sensory ganglia, and (2) vagotomy abrogates endotoxin-induced Fos expression in these ganglia. Male rats, which had previously received vagotomy or sham surgery, were injected intraperitoneally or intravenously with either endotoxin or saline. Fos immunolabeling was absent in saline-treated rats. In contrast, scattered cells within the vagal sensory ganglia showed Fos immunoreactivity after both intraperitoneal and intravenous endotoxin administration in sham-operated rats. Vagotomy abolished Fos expression after intraperitoneal endotoxin administration, whereas after intravenous administration Fos expression was strongly attenuated, but not eliminated. These findings implicate vagal afferents as a potential signaling pathway to brain regions that generate illness responses to pro-inflammatory mediators.

Animals↗
PubMedDate not supplied

ACTH response to a low dose but not a high dose of bacterial endotoxin in rats is completely mediated by corticotropin-releasing hormone.

In experimental animals and humans, bacterial endotoxin activates the hypothalamus-pituitary-adrenal (HPA) axis. The pathways by which endotoxin stimulates adrenocorticotropic hormone (ACTH) and corticosterone secretion are uncertain. In the present study we compared the role of hypothalamic corticotropin-releasing hormone (CRH) in the activation of the HPA axis by a low (2.5 micrograms/kg) and a high (2.5 mg/kg) dose of bacterial endotoxin. Two experimental models were applied using chronically cannulated male Wistar rats. In the first model, rats were subjected to lesions of the hypothalamus that interrupted dorsal, lateral and frontal input to the median eminence (anterolateral deafferentation) or to sham operation and rats were used 7 days later. Before and at hourly intervals after endotoxin (2.5 micrograms/kg i.p.), blood samples were taken for the determination of plasma ACTH and corticosterone concentrations. Deafferentation of the hypothalamus strongly attenuated the elevations in plasma ACTH and corticosterone concentrations by a low dose of endotoxin compared to the responses in sham-operated animals. The second model involved passive immunization to CRH using a monoclonal antibody to rat/human CRH (PFU83). PFU83 (90 nmol/rat) abolished the elevation of plasma ACTH concentrations and attenuated corticosterone responses to a low dose of endotoxin (2.5 micrograms/kg i.p.) compared to that in control IgG-treated rats. Since the corticosterone responses to endotoxin were less effectively inhibited by the antibody than the ACTH responses, we postulate that non-ACTH-dependent mechanisms may contribute to the corticosterone response to endotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗