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Biomedical subjects

L E Ericson

Publications and source records attributed to L E Ericson.

At least 91 records · Page 5Linked to original sources
PubMed1984

Turnover of apical plasma membrane in thyroid follicle cells of normal and thyroxine-treated rats.

In thyroid follicle cells exocytotic vesicles transfer newly synthesized thyroglobulin to the follicle lumen and new membrane to the apical plasma membrane. In a previous study data obtained by quantitative electron microscopy were used to estimate the turnover of the pool of exocytotic vesicles in follicle cells of normal and thyroxine-treated (2 days) rats. In the present study, these kinetic data were combined with stereological measurements to calculate the amount of membrane added to the apical plasma membrane by exocytosis and, indirectly, to estimate the turnover of this membrane. In follicle cells of normal rats the area of the membrane added was about 240 micron2/h (180 micron2/h after correction for stereological overestimation) and in thyroxine-treated rats about 105 micron2/h (corrected 80 micron2/h). These areas corresponded to the addition of 1.2% and 0.7% respectively, of the apical plasma membrane per minute. In each cell the total volume of the exocytotic vesicles emptying their content into the follicle lumen in normal rats was 6.2 micron3/h (corrected 4.7 micron3/h) and in thyroxine-treated rats 3.0 micron3/h (corrected 2.3 micron3/h). Considerations based on the findings in the present study suggest that in normal rats macropinocytosis (formation of colloid droplets) is the most important endocytotic pathway for internalization of colloid, while micropinocytosis is the major pathway of membrane internalization. In thyroxine-treated rats macropinocytosis is inhibited. The low volume capacity of the micropinocytotic pathway probably explains the accumulation of colloid protein, mainly thyroglobulin, observed in such rats.

Animals↗
PubMed1984

Rate of protein transport in thyroid follicle cells of normal, thyroxine-treated and TSH-injected rats.

The transport of labeled protein in thyroid follicles was studied with quantitative electron microscopic autoradiography in normal and T4-treated rats (2d) injected with 3H-leucine 1 to 6 h before perfusion fixation. During this time interval the total amount of labeled protein in either group was unchanged, although T4-treatment caused a reduction by about 30% of the amount of 3H-leucine incorporated into protein. The autoradiographic data were corrected for the effect of scatter of radioactivity. The relative amounts of labeled, exportable protein in the compartments Er-Golgi and exocytotic vesicles were then estimated. The half-lives of labeled, exportable protein in these compartments were calculated with non-linear regression analysis. In normal rats the half-life of labeled, exportable protein in ER-Golgi was 28 min and in the exocytotic vesicles 18 min. Inhibition of TSH-secretion by injection of thyroxine decreased the rate of protein transport through the follicle cell and increased the half-lives to 63 min (ER-Golgi) and 62 min (exocytotic vesicles). TSH given to thyroxine-treated rats 20 min or 1.5 h before fixation reduced the half-lives of labeled, exportable protein in ER-Golgi to 25 to 33 min and in exocytotic vesicles to 9 min. The findings indicate that TSH regulates the rate of intracellular protein transport in rat thyroid follicle cells at the exocytotic step as well as at an earlier step in the pathway of intracellular protein transport. The mechanism and exact location of the latter TSH regulated step is at present unknown.

Animals↗
PubMed1983

The effect of thrombocytopenia and antiserotonin treatment on the lodgement of circulating tumor cells. A vital fluorescence microscopic, electron microscopic and isotope study in the rat.

The hepatic lodgement of intraportally injected fibrosarcoma cells was analysed with a combination of vital fluorescence microscopic, electron microscopic and isotope techniques in normal, thrombocytopenic and antiserotonin treated (Ketanserin) rats. Ketanserin had no effect on the initial arrest of the tumor cells, as measured 5 min after tumor cell injection, which is in analogy with our previous results on thrombocytopenia. Three hours after injection, the number of lodged tumor cells was significantly reduced by both thrombocytopenia and Ketanserin treatment. Thrombocytopenia was more efficient in reducing tumor cell lodgement than antiserotonin treatment. The in vivo and electron microscopic observations indicated that the reduction of tumor cell lodgement was due to an increased destruction of tumor cells. The similar effects of Ketanserin and thrombocytopenia suggest that serotonin, when released from platelets activated in the presence of tumor cells, increases the survival of fibrosarcoma cells lodged in the liver.

Animals↗
PubMed1983

The arrest of circulating tumor cells in the liver microcirculation. A vital fluorescence microscopic, electron microscopic and isotope study in the rat.

Previous studies have shown that thrombocytopenia reduces the lodgement of circulating tumor cells, thus indicating a role of platelets in tumor cell lodgement. In this study, a vital fluorescence microscopic technique, electron microscopy and isotope measurements were combined to analyse the very first phase (5 min) of tumor cell lodgement using a syngeneic, methylcholantrene induced fibrosarcoma. The mode of tumor cell arrest in the liver microvasculature of normal and thrombocytopenic rats was studied. In addition, tumor cell size and deformability were investigated in vitro. The in vitro experiments showed that the fibrosarcoma cells were very rigid. Both the vital microscopic and electron microscopic studies indicated that the tumor cells mainly became arrested by mechanical trapping in narrow liver sinusoids. Arrest of tumor cells by adherence to venular walls was a rare finding. Platelets did not seem to influence any of these initial phenomena of tumor cell lodgement. The isotope measurements, which showed no difference in the number of tumor cells lodged in the liver between normal and thrombocytopenic rats, further indicated that the initial arrest of the fibrosarcoma cells was not influenced by platelets.

Animals↗
PubMed1983

Heart lesions in the frog at high environmental temperature.

Frogs (R. pipiens) adapted to 12 degrees C were exposed to increased environmental temperature during 2 hr. At 33 degrees C gross heart lesions started to appear in a few cases and at 37 degrees C, 71% of the frogs showed ventricular aneurysms and some died. Critical thermal maximum (CTM) was around 37 degrees C in autumn, winter and early spring, whereas in late spring and summer CTM was at 39 degrees C and during these last-mentioned periods of the year gross heart lesions at high temperature did not start until at 37 degrees C. After 2 hr at 37 and 39 degrees C respectively, ECG-abnormalities occurred indicating myocardial injury. Isolated strips of the heart ventricle from frogs with gross heart lesions showed a deteriorated resistance towards cyanide anoxia as measured by an isometric procedure. The ultrastructure was deranged by the high temperature, the changes mainly involving the mitochondria and the myofibrils. These alterations were focal but depletion of glycogen particles was diffuse. As the high temperature induced changes similar to those provoked by catecholamines, propranolol was given in some frogs before the heat exposure. This beta-adrenoceptor blockade did only reduce some of the abnormal changes by 37 degrees C.

Animals↗
PubMed1983

Selective macropinocytosis of thyroglobulin in rat thyroid follicles.

We have explored the possibility that pseudopods might provide a mechanism by which newly synthesized, hormone-poor thyroglobulin recently delivered to the follicle lumen escapes immediate reuptake and degradation. The study was performed with electron microscopic autoradiography on rats pretreated with T4 for 2 days and injected with [3H]leucine or Na125I. Pseudopods were induced by the injection of TSH (100 mU) 20 min before perfusion fixation. The density of autoradiographic grains in colloid droplets located in pseudopods was compared with the grain density in different regions of the follicle lumen. In rats injected with radioleucine 1.5 or 3 h before TSH injection, the grains were distributed in a gradient in the lumen periphery. Seventy to 80% of the grains were located over the microvillus region. The grain density over colloid droplets in pseudopods was about 10% of that over the microvillus region and similar to the density at a distance 1-2 microns from the microvillus region. After injection of Na125I, 40 min before TSH, the grains were more widely spread in the lumen, but still formed a gradient in the lumen; about 30% of the grains were associated with the microvillus region. Again, the grain density over colloid droplets in pseudopods was about the same as that at a distance 1-2 microns from the microvillus region. Our observations are compatible with the idea that pseudopods collect thyroglobulin located at some distance from the apical surface. This, together with the circumstance that newly synthesized thyroglobulin is located close to the apical plasma membrane, might provide a mechanism of selective macropinocytosis by which newly synthesized thyroglobulin recently delivered to the follicle lumen is prevented from immediate reuptake.

Animals↗
PubMed1982

The healing of frog heart lesions induced by isoproterenol injections.

Isoproterenol (IPR) induces myocardial lesions in R. pipiens adapted to +25 degrees C, but not to +8 degrees C. The spontaneous healing of these lesions in the form of ventricular wall aneurysms occurs during the first three weeks after IPR, and the ultrastructure of the myocardial cells in fully restored from the fourth week after IPR. Leukocytes, adhering to the lacunar endothelium and including phagocytic vacuoles, appear 8-15 days after IPR. Severely altered heart muscle cells then contain myelin figures or a pyknotic nucleus. In the acute stage of the IPR-lesions, heart muscle preparations from the ventricular wall show a very lowered resistance towards cyanide anoxia as judged from the isometric force decay. During the seven weeks of observation after IPR the resistance to cyanide anoxia is continuously improved almost to normal values. Thus restoration of structure and function occurs in parallel.

Animals↗
PubMed1981

Adrenergic innervation of pancreatic islets and modulation of insulin secretion by the sympatho-adrenal system.

Morphological changes in the adrenergic innervation of pancreatic islets after chemical sympathectomy by use of 6-hydroxydopamine and the influence of the sympatho-adrenal system on insulin secretion were investigated in the mouse and rat. Fluorescence histochemistry revealed a clear-cut reduction in the number of adrenergic nerve fibres in the pancreatic islets 2 days after administration of 6-hydroxydopamine; the reduction was more pronounced in the rat than in the mouse. In the rat, a partial regeneration was seen after 6 weeks. In the pancreas of the mouse, after administration of 6-hydroxydopamine, a severe damage of unmyelinated nerve fibres was revealed electron microscopically. However, no ultrastructural or immunohistochemical alterations could be demonstrated in the endocrine cells of the islets. 6-Hydroxydopamine induced a depression of basal plasma insulin concentrations in mice and an elevation in rats. Adrenalectomy depressed basal plasma insulin levels in mice. The alpha-adrenoceptor antagonist phentolamine enhanced insulin secretion in normal mice. The secretory response of insulin to phentolamine was diminished by chemical sympathectomy and almost abolished by adrenalectomy or the combination of chemical sympathectomy and adrenalectomy. Thus, the effect of phentolamine is probably mediated by liberated catecholamines. It is concluded that basal insulin secretion is partially regulated by the sympatho-adrenal system and that species differences exist in this respect. In addition, the results suggest that endogenous catecholamines have the ability to promote insulin secretion.

Adrenal Cortex↗
PubMed1981

Effect of graded doses of thyrotropin on exocytosis and early phase of endocytosis in the rat thyroid.

Our previous studies on the follicle cell have shown that exocytosis and endocytosis induced by a large dose of TSH (500 mU) are functionally related elements of a redistribution of membrane in the apical cell region. To explore the significance of exocytosis at submaximal levels of stimulation, T4-treated rats were injected iv with 5 or 50 mU TSH 5, 10, or 20 min before perfusion fixation of the thyroid. Additional groups were given 20 or 100 mU TSH or saline 20 min before fixation. Electron microscopic stereology showed that TSH induced exocytosis and endocytosis and a redistribution of membrane in the apical part of the follicle cell. Exocytosis preceded endocytosis. The redistribution of membrane was quantitatively different but qualitatively similar to that previously observed after a large dose of TSH. The rate of exocytosis was linearly correlated with the logarithm of the TSH dose. The size, but not the number (counted in the light microscope), of pseudopods was related to the TSH dose; at 20 min, the membrane surface area of a pseudopod induced by 100 mU was about twice that of a pseudopod induced by 5 mU. The total membrane surface area of endocytotic structures (pseudopods, colloid droplets, and micropinocytotic vesicles) was related to the surface area of the membrane added to the apical plasma membrane by exocytosis. The findings indicate that exocytosis is part of the normal response of the follicle cell to stimulation and represents the first step in the redistribution of membranes in the apical part of the follicle cell induced by TSH. At all levels of stimulation, the membrane of the exocytotis vesicles, rather than the apical plasma membrane, is the membrane reserve used to make endocytotic structures. (Endocrinology 108: 399, 1981)

Animals↗
PubMed1978

beta-Adrenergic insulin release and adrenergic innervation of mouse pancreatic islets.

An investigation of the stereospecificity of beta-adrenergic insulin release, its relation to alpha-adrenergic blockade and the adrenergic innervation of the pancreatic islets was performed in the mouse. It was observed that in vivo beta-adrenergic stimulation of insulin release by isopropylnoradrenaline was stereospecific for the L-stereoisomer and selectively blocked by the L-isomer of the beta-adrenergic antagonist L-propranolol. D-propranolol had no effect. Pretreatment of mice with a dose of D-isopropylnoradrenaline devoid of insulin releasing activity, slightly increased the subsequent insulin response to a half-maximal dose of L-isopropylnoradrenaline. Basal insulin secretion was blocked by L-propranolol (beta-adrenergic blockade) and increased by phentolamine (alpha-adrenergic blockade). A beta-blocked insulin response to L-isopropyl-noradrenaline could be overcome by alpha-adrenergic blockade depending on the dose of the beta-agonist, suggesting a close association between the adrenergic receptors. The adrenergic innervation of the islet cells was studied by electron microscopic autoradiography after injection of 3H-L-noradrenaline. It was observed that labelled adrenergic nerve terminals were associated with both A1- (D-), A2- and B-cells. The nerves were mainly distributed in the periphery of the islets either as single axons or as bundles. The majority of the terminals were associated with A2-cells, the most frequent cell type in the islet periphery. However, in all islets examined terminals were found close to B-cells. Adrenergic terminals often caused indentations in the contour of an islet cell and were separated from the islet cell membrane only by a narrow intercellular space, about 20 nm in width. It is concluded that the islet cells of the mouse are equipped with the morphological substrate for direct adrenergic regulation. Further it is suggested that the B-cell is supplied with L-stereospecific beta-adrenergic receptors and that the alpha- and beta-adrenergic receptors are at least partially interrelated.

Adrenergic Fibers↗