PubMed Health⌕ Search

Biomedical subjects

L E Ericson

Publications and source records attributed to L E Ericson.

At least 109 records · Page 6Linked to original sources
PubMed1978

Effects of thyrotropin on thyroglobulin exocytosis and iodination in the rat thyroid gland.

Rats, pretreated with thyroxine for 2 days, were given one or two iv injections of 500 mU of TSH; in some groups the second TSH dose was replaced by 0.75 micronmol isoproternol. The effects of the thyroid stimulators on the following parameters were studied: the number of exocytotic vesicles in the follicle cells; the incorporation of 125I into thyroid proteins, measured over periods of 5 min; and the thyroidal cAMP contents. At 2 h after TSH administration, a second dose of TSH failed to stimulate iodination while at 8 h the iodination response was "normal". Two hours after TSH the follicle cells contained practically no exocytotic vesicles but at 8 h they had a full supply of vesicles, and this was emptied by the second TSH injection. THE CAMP content was less increased by the second TSH injection than by the first one, but the stimulatory effect of the second TSH dose on cAMP was the same at 2 h and at 8 h; this indicates that the lack of iodination response at 2 h was not simply due to blocking of TSH receptors. Isoproternol, which acts on other receptors than does TSH, cause a similar cAMP increase incontrols and at 2 h and 8 h after TSH, but stimulated iodination only in controls and at 8 h after TSH; this supported the conclusion that the lack of iodination response to a second TSH dose at 2 h was not due to impairment of the adenylate cyclase-cAMP system. These observations taken together strongly indicate that a rapid iodination response to TSH depends on stimulated exocytosis which, in turn, requires a pool of exocytotic vesicles in the follicle cells. Such a coupling between exocytosis and iodination seems appropriate since by exocytosis uniodinated thyroglobulin and membrane, showing peroxidase activity histochemically, are delivered to the site of iodination, the apical cell surface.

Animals↗
PubMed1978

Quantitative electron microscopic studies on exocytosis and endocytosis in the thyroid follicle cell.

The effect of TSH (0.5 U), given iv to T4-treated rats, on the distribution of membranes in the apical part of the thyroid follicle cell was investigated by electron microscopic morphometry. In unstimulated cells, the membrane surface area of exocytotic vesicles (Ev) was slightly larger than that of the apical plasma membrane; the latter had an estimated surface area of 180-190 micron2/follicle cell. Three phases in the action of TSH could be discerned. A first phase (up to 5 min) was dominated by exocytosis; the membrane surface area of Ev decreased by about 40% and the apical plasma membrane showed a corresponding increase; pseudopods were rare. A second phase (5-20 min) was characterized by an increase in the membrane surface area of pseudopods while the area of Ev and apical plasma membrane decreased. A third phase (20-30 min) was characterized by a decrease in the membrane surface area of the pseudopods and an equivalent increase in the membrane surface area of colloid droplets. The total membrane surface area measured was about the same in all groups of rats. The membrane surface area of endocytotic structures (pseudopods and colloid droplets) at 20 and 30 min was about the same as that of the apical plasma membrane in unstimulated cells. The present results are consistent with the hypothesis that after stimulation of the thyroid follicle cell, membrane is first transferred from Ev to the apical plasma membrane. From the enlarged apical plasma membrane, pseudopods are formed. Membrane from pseudopods is then internalized in the form of colloid droplets.

Animals↗
PubMed1978

Blood capillary enlargement during the development of thyroid hyperplasia in the rat.

To study blood capillary growth in the hyperplastic thyroid gland, rats were fed 0.25% thiouracil in a low iodine diet for time intervals up to 100 days. Thyroids were fixed by vascular perfusion and embeded in Epon. Whole lobes were sectioned from pole to pole and slides were prepared of sections every 0.3 mm. Capillaries were clearly enlarged by 3 days and they enlarged progressively thereafter. By 3 days, the cells of many neighboring capillaries came into close apposition and from this time on, there was evidence of fusion of capillary walls in the form of partial septa in the capillary lumens. Fusion continued until 20 days, when follicles were almost completely surrounded by a continuous endothelial sheet and unfused capillary walls were separated by connective tissue. The vascular pattern around peripheral follicles changed in a way similar to interior follicles, except that in places, capillaries were gradually excluded from the space between epithelium and thyroid capsule. Vascular enlargement was restricted to the thyroid blood vessels. There was no obvious enlargement of the blood capillaries of the parathyroid despite its close proximity to the thyroid.

Animals↗
PubMed1977

Accumulation of dopamine in mouse pancreatic B-cells following injection of L-DOPA. Localization to secretory granules and inhibition of insulin secretion.

Accumulation and subcellular localization of dopamine (DA) in pancreatic B-cells and its effects on insulin secretion were investigated in mice following a single injection of L-3,4-dihydroxyphenylalanine (L-DOPA). Electron microscopic autoradiography showed that 3H-DA formed from administered 3H-DOPA was present over B-cells as well as over other types of islet cells. Pretreatment of the animals with a decarboxylase inhibitor greatly reduced the number of autoradiographic grains. In the B-cells the 3H-DA-grains were associated with the secretory granules. The location of the label may suggest an incorporation in the periphery of the beta-granule, rather than in the dense core, supposed to contain insulin. Accumulation of DA in the B-cells following L-DOPA administration was found to inhibit partially the insulin secretory response to different insulin secretagogues (glucose, glibenclamide and L-isopropylnoradrenaline (L-IPNA). Treatment with monoamine oxidase inhibitor + L-DOPA induced an almost total suppression of L-IPNA-stimulated insulin secretion, whereas glucose-induced insulin release was still only partially inhibited. Pretreatment with a decarboxylase inhibitor abolished the effects of L-DOPA. It is suggested that intracellularly accumulated DA in the B-cell exerts an inhibitory action on insulin releasing mechanisms induced by different secretagogues and that this action might involve interference with a calcium translocation process at the level of the secretory granule.

Animals↗
PubMed1977

Ultrastructural and functional aspects of frog heart lesions after isoproterenol.

The purpose of the present study was to explore the possible correlation between the ultrastructural changes and the functional changes induced by isoproterenol (IPR) in the myocardium of the frog. The study was performed on winter frogs (R. pipiens), The experimental animals wend then given 2 daily doses of IPR (200 mg/kg b,w.). Twenty-four hours after the second IPR dose, specimens were taken from the heart ventricle and subjected to electron microscopical examination and to analysis of the isometric force decay in response to anoxia produced by sodium cyanide. Specimens were taken from macroscopically non-damaged portions of the ventricle as well as from aneurysms. Control animals were kept at + 8 degrees C and + 25 degrees C and injected with saline. In all IPR-injected animals the specimens from macroscopically non-damaged parts of the myocardium showed ultrastructural changes characterized by a relative increase in mitochondrial mass and a pronounced reduction of glycogen. Specimens from aneurysms showed similar changes but in some fibres signs of more severe injury were observed such as fragmentation of the cristae of the mitochondria and disintegration of myofibrils. The functional analyses showed that the isometric force decay of the heart muscle strips induced by the respiratory block by cyanide was much greater in specimens from IPR-treated animals than in those from control frogs. The augmented force decay was found in both strips from macroscopically normal parts of the myocardium and in those from aneurysms although it was somewhat greater and more rapid in the latter. The observed, minor functional difference between macroscopically non-damaged portions of the myocardium and aneurysms is remarkable with respect to the different preservation of myofilaments in these regions. This similarity in functional decline could possibly be due to the observed homogenous reduction of glycogen in the IPR-exposed myocardium since glycogen was the only source of ATP under the experimental conditions of current interest.

Animals↗
PubMed1977

Protein concentration of the rat thyroid colloid during thyroxine treatment.

Sprague-Dawley rats were given daily doses of 20 mug thyroxine for varying periods between 1 and 21 days. Samples of colloid were obtained by micropuncture in vivo of follicles in the thyroid isthmus. The protein content of the samples was determined by gel electrophoresis and the volume by a technique based on radioactivity measurement. The relative volume of the follicle lumina was determined by light microscopy. Treatment with thyroxine resulted in an increase in the protein concentration of the colloid. This increase was statistically significant after 2 days and the concentration remained elevated throughout the experimental period. The size of the follicle lumina also increased, most rapidly during the first week. It is suggested that the increase in protein concentration of the colloid during thyroxine treatment is due to inhibition of endocytosis of colloid in combination with the discharge into the follicle lumen of highly concentrated protein.

Animals↗
PubMed1977

Early effects of thyroid stimulating hormone (TSH) on exocytosis and endocytosis in the thyroid.

The early effect (3 min) of thyroid stimulating hormone (TSH) on exocytosis-endocytosis in the rat thyroid follicle cell was investigated by electron microscopic morphometry. All rats used were pre-treated with thyroxine for 2 days prior to the experiments. In control rats, the membrane surface area of exocytotic vesicles, the only type of vesicle present in the apical part of the follicle cell, approximately equaled that of the apical plasma membrane. Intravenous administration of TSH caused a significant decrease in the membrane surface area of exocytotic vesicles by about 20% and a corresponding, significant increase in the membrane surface area of the apical plasma membrane by about 20%. Pseudopods were present in 4 of 6 TSH-injected rats examined, but the membrane surface area of these structures was only 15% of the increase in the surface area of the apical plasma membrane. The total membrane surface area analyzed was not influenced by injection of TSH. We conclude that the initial effect of TSH on the thyroid follicle cell is a re-distribution of membrane from exocytotic vesicles to the apical plasma membrane. This conclusion is in harmony with our previous observations which indicate that the (membrane-requiring) endocytotic response after TSH is regulated by the amount of membrane material added to the apical plasma membrane by exocytosis.

Animals↗
PubMed1975

Effect of vinblastine in vivo on ultrastructure and insulin releasing capacity of the B-cell following sulphonylurea and isopropyl-noradrenaline.

The effect of vinblastine in vivo on ultrastructure and insulin releasing capacity of the B-cell was studied in mice. Treatment with vinblastine (1.1 mumole/mouse) resulted in a 75% decrease of the amount of normal microtubules and the appearance of characteristic paracrystals. Basal plasma immunoreactive insulin levels were depressed to about 60% of the control level. The dose-response pattern for insulin release (first phase) following two chemically unrelated insulin secretagogues, the potent sulphonyl-urea derivative, glibenclamide, and the beta-adrenegic agonist L-isopropylnoradrenaline, (L-IPNA), was tested with and without vinblastine pretreatment. The dose-response curves for L-IPNA-induced insulin release in vinblastine-treated and control animals did not deviate significantly from each other, whereas insulin release following glibenclamide was almost totally suppressed by vinblastine except at the lowest dose level. Injection of maximal doses of glibenclamide or L-IPNA did not alter the ultrastructural changes induced by vinblastine in the B-cells. It is suggested that the microtubular system of the B-cell might play a minor role for certain insulin-releasing processes and/or that vinblastine might have other important effects on the insulin secretory machinery.

Animals↗
PubMed1975

Exocytosis of protein into the thyroid follicle lumen: an early effect of TSH.

As shown in a preceding paper, only exocytotic vesicles conveying newly synthesized protein to the follicle lumen remain in the apical part of rat thyroid follicle cells following elimination of TSH secretion. In the present paper the effect of TSH on these exocytotic vesicles was investigated. TSH secretion was suppressed by administration of thyroxine for 2 days. In the electron microscope administration of TSH was seen to induce well-known signs of endocytosis, such as formation of pseudopods and colloid droplets. In addition, a previously unrecognized change was noted, namely a progressive decrease in the number of exocytotic vesicles. At 5 min after TSH the number was obviously reduced and at 20 min less than 10% of the original number of vesicles remained. Quantitative electron microscopic autoradiography after administration of [3H]leucine showed that TSH caused, concomitant with the disappearance of vesicles, a transfer of radioactivity from the apical region of the follicle cell to the periphery of the follicle lumen. The distribution of labeled protein in thyroid subcellular fractions was studied 1.5 h after administration of [14C]leucine. At 5 min after administration of TSH there was an increase of protein-bound label in the supernatant fraction, containing the luminal colloid, and a corresponding decrease of label in the particle fraction which contained most of the cell organelles, including the exocytotic vesicles. This TSH-induced redistribution of labeled proteins was more pronounced at 10 min and still more at 20 min and appeared to be dose-dependent. These observations taken together are considered to justify the conclusion that TSH induces transfer of newly synthesized protein from the follicle cells to the follicle lumen by exocytosis (i.e., emptying of specific apical vesicles). It is suggested that a causal and functional interrelation may exist between the exocytotic and endocytotic processes.

Animals↗
PubMed1975

Influence of histamine- and 5-hydroxytryptamine-containing thyroid mast cells on thyroid blood flow and permeability in the rat.

The possible significance of thyroid mast cells in the regulation of thyroid blood flow and capillary permeability was investigated in rats whose TSH secretion had been eliminated by exogenous T4. Mast cells were identified by their abundance of metachromatic granules, and their content of histamine and 5-hydroxytryptamine (5-HT) was examined by fluorescence histochemistry. Thyroid histamine levels were determined by fluorometry. The tissue uptake of 86Rb was used as an indicator of blood flow and permeability. Numerous histamine- and 5-HT-containing mast cells were found within the thyroid and in connective tissue adjacent to the thyroid, whereas juxtathyroidal muscle tissue was virtually devoid of mast cells. Administration of compound 48/80 evoked a prompt depletion of 5-HT, histamine and metachromatic granules from thyroid mast cells, and a concomitant increase in the thyroidal uptake of 86Rb. The 86Rb uptake by juxtathyroidal muscle tissue was unaffected. Exogenous 5-HT and histamine both induced prompt increments in thyroidal 86Rb uptake, and 5-HT also stimulated 86Rb uptake in juxtathyroidal muscle tissue. TSH, previously shown to induce a gradual amine release from mast cells within, but not outside, the thyroid, evoked a gradual increase in thyroidal, but not in muscular, uptake of 86Rb. The findings support the concept that, in the rat, histamine and/or 5-HT, released from intrathyroidal mast cells by TSH, stimulate thyroid blood flow and/or permeability.

Animals↗