Electrical responses of cultured thyroid cells to serotonin

1985 ◽  
Vol 107 (3) ◽  
pp. 397-401 ◽  
Author(s):  
P. A. McGrath ◽  
J. R. Bourke ◽  
G. J. Huxham ◽  
S. W. Manley
Keyword(s):  
Membrane Potential ◽  
Cyclic Amp ◽  
Resting Membrane Potential ◽  
Previous Exposure ◽  
Dibutyryl Cyclic Amp ◽  
Thyroid Cells ◽  
Adrenoceptor Agonist ◽  
Electrical Responses

ABSTRACT Cultured porcine thyroid cells, maintained in the differentiated state by dibutyryl cyclic AMP, responded to serotonin (5-HT; 10 nmol/l to 1 μmol/l) with a depolarization of the membrane potential, but did not respond to histamine (100 μmol/l) or dopamine (1 μmol/l). The resting membrane potential of these cells was about − 71 mV, maximal concentrations of 5-HT (1 μmol/l) inducing a depolarization to approximately −53 mV. Methysergide or phenoxybenzamine, but not propranolol, abolished the response to 5-HT. Sensitivity to 5-HT was reduced by previous exposure of cultures to TSH, the β-adrenoceptor agonist salbutamol or 5-HT itself. J. Endocr. (1985) 107, 397–401

Effect of epidermal growth factor on the membrane potential of cultured porcine thyroid cells

1986 ◽  
Vol 109 (3) ◽  
pp. 321-324 ◽  
Author(s):  
J. R. Bourke ◽  
P. A. McGrath ◽  
G. J. Huxham ◽  
M. J. Waters ◽  
S. W. Manley
Keyword(s):  
Membrane Potential ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cyclic Amp ◽  
Follicle Cells ◽  
Dibutyryl Cyclic Amp ◽  
Thyroid Cells ◽  
Epidermal Growth

ABSTRACT Cultured porcine thyroid cells maintained in media containing TSH exhibited a membrane potential of −50 mV, and hyperpolarized by about 10 mV within 1 h of the addition of epidermal growth factor (EGF; 10 ng/ml). Follicle cells had depolarized to −45 mV after 4 h of exposure to EGF. Cells maintained in dibutyryl cyclic AMP (dbcAMP) did not alter their membrane potential when exposed to EGF for up to 4 h. Cultures washed to remove the TSH or dbcAMP hyperpolarized to − 75 mV within 30 min, and a reversible depolarization to − 60 mV was observed on addition of EGF. It was concluded that EGF acts as a physiological antagonist of TSH and also exerts a separate depolarizing influence on cultured thyroid cells. J. Endocr. (1986) 109, 321–324

CHANGES IN MEMBRANE POTENTIAL OF CULTURED PORCINE AND HUMAN THYROID CELLS IN RESPONSE TO THYROTROPHIN AND OTHER AGENTS

1981 ◽  
Vol 88 (2) ◽  
pp. 187-NP ◽  
Author(s):  
J. R. BOURKE ◽  
K. L. CARSELDINE ◽  
S. H. FERRIS ◽  
G. J. HUXHAM ◽  
S. W. MANLEY
Keyword(s):  
Membrane Potential ◽  
Cyclic Amp ◽  
Human Thyroid ◽  
Resting Membrane Potential ◽  
Prostaglandin E ◽  
Follicular Cells ◽  
Thyroid Cells ◽  
Enhanced Sensitivity ◽  
Long Acting ◽  
Cells Cultured

Thyrotrophin (TSH), cyclic AMP, cyclic GMP and 1-methyl-3-isobutyl-xanthine (MIX) promoted the reassociation of isolated porcine and human thyroid cells into follicular structures in culture and stimulated the uptake of radio-iodide. Monolayer cells were present in all cultures, but in decreasing proportions as the concentration of stimulator was increased. The resting membrane potential of porcine thyroid cells cultured for 4 days in the presence of TSH was −54 ± 3·6 (mean ± s.d.) mV for follicular cells and −31 ± 2·6 mV for monolayer cells. In the absence of TSH, only monolayer cells were present and their membrane potential was −24 ± 2·0 mV. Removal of hormone by washing resulted in hyperpolarization to −70 ± 2·9 mV (follicular cells) or −59 ± 3·4 mV (monolayer cells). Subsequent replacement of TSH, or addition of cyclic AMP, MIX, prostaglandin E1 (PGE1) or long-acting thyroid stimulator immunoglobulin resulted in depolarization of previously hyperpolarized cells, to approximately the membrane potential observed before washing. Incubation in MIX resulted in enhanced sensitivity to the depolarizing effect of TSH. Cells cultured in the absence of TSH were unresponsive to TSH or other stimulators. The membrane potential of human thyroid cells behaved similarly in response to TSH, to hormone removal and replacement, and to MIX and PGE1.

Regulation of the astrocyte resting membrane potential by cyclic AMP and protein kinase A

Glia ◽  
2006 ◽  
Vol 54 (4) ◽  
pp. 316-328 ◽  
Author(s):  
Sally Bolton ◽  
Kirsty Greenwood ◽  
Nicola Hamilton ◽  
Arthur M. Butt
Keyword(s):  
Membrane Potential ◽  
Protein Kinase ◽  
Cyclic Amp ◽  
Protein Kinase A ◽  
Resting Membrane Potential ◽  
Kinase A

Sodium dependence of the thyrotrophin-induced depolarization in cultured porcine thyroid cells

1986 ◽  
Vol 108 (2) ◽  
pp. 225-230 ◽  
Author(s):  
T. A. Hambleton ◽  
J. R. Bourke ◽  
G. J. Huxham ◽  
S. W. Manley
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Potassium Concentration ◽  
Sodium Current ◽  
Resting Membrane Potential ◽  
Thyroid Cell ◽  
Free Medium ◽  
Thyroid Cells ◽  
Voltage Dependent ◽  
Sodium And Potassium

ABSTRACT Cultured porcine thyroid cells exhibit a resting membrane potential of about − 73 mV and depolarize to about − 54 mV on exposure to TSH. The depolarizing response to TSH was preserved in a medium consisting only of inorganic salts and buffers, but was abolished in sodium-free medium, demonstrating dependence on an inward sodium current. Increasing the potassium concentration of the medium resulted in a reduction in the resting membrane potential of 60 mV per tenfold change in potassium concentration, and a diminished TSH response. A hyperpolarizing TSH response was observed in a sodium- and bicarbonate-free medium, indicating that a hyperpolarizing ion current (probably carried by potassium) was also enhanced in the presence of TSH. Tetrodotoxin blocked the TSH response. We conclude that the response of the thyroid cell membrane to TSH involves increases in permeability to sodium and potassium, and that the thyroid membrane ion channels bear some similarity to the voltage-dependent sodium channels of excitable tissues, despite the absence of action potentials in the thyroid. J. Endocr. (1986) 108, 225–230

IN-VITRO STUDIES OF NORMAL HUMAN THYROID CELLS: RESPONSES TO THYROTROPHIN AND DIBUTYRYL CYCLIC AMP

1977 ◽  
Vol 72 (1) ◽  
pp. 87-96 ◽  
Author(s):  
S. P. BIDEY ◽  
P. MARSDEN ◽  
J. ANDERSON ◽  
C. G. McKERRON ◽  
H. BERRY
Keyword(s):  
Cyclic Amp ◽  
Thyroid Tissue ◽  
Three Dimensional ◽  
Human Thyroid ◽  
Dibutyryl Cyclic Amp ◽  
Iodide Uptake ◽  
Thyroid Cells ◽  
Normal Human

SUMMARY Follicular cells isolated from normal human thyroid tissue have been cultured for up to 140 h with bovine thyrotrophin (TSH) or dibutyryl cyclic AMP (DBcAMP). Both compounds induced marked reorganization of the cells into three-dimensional follicular structures, whilst non-supplemented cells assumed a monolayer form. Cultures treated initially with TSH or DBcAMP showed a greater iodide uptake capacity, in comparison with unsupplemented cultures, in which iodide uptake was markedly diminished after 24 h. The release of tri-iodothyronine (T3) and thyroxine (T4) into the medium was determined by radioimmunoassay. Both TSH- and DBcAMP-treated cells showed a significant increase in iodothyronine output compared with unsupplemented control cells. In contrast to the 'classical' TSH-induced depression of the T4:T3 ratio in vivo, an increase in the ratio was observed for both TSH- and DBcAMP-supplemented cells in vitro. The ratio was also significantly greater after TSH than after DBcAMP, and possible implications of this finding are discussed.

Refractoriness of TSH- and PGE2-stimulated iodine metabolism in cultured porcine thyroid cells, evidence for refractoriness at the level of cAMP action

1982 ◽  
Vol 99 (4) ◽  
pp. 530-539 ◽  
Author(s):  
Nobuyuki Takasu ◽  
Akira Sato ◽  
Takashi Yamada ◽  
Yoshifusa Shimizu
Keyword(s):  
Cyclic Amp ◽  
Chronic Exposure ◽  
Regulatory Mechanism ◽  
Iodine Uptake ◽  
Previous Exposure ◽  
Acute Effects ◽  
Thyroid Cells ◽  
Iodine Metabolism ◽  
Do So

Abstract. In an attempt to study intrinsic regulatory mechanism involved in iodine metabolism, chronic and acute effects of TSH, PGE2 and DBC on iodine uptake, iodide discharge and organic binding of iodine were examined using cultured porcine thyroid cells. Culture in the presence of TSH, PGE2 and DBC for 6 days maintained the ability of thyroid cells to take up iodide and organify it, but culture in the absence of these substances failed to do so. When incubated with Nal in the presence of 1 mm methylmercaptoimidazole (MMI), the cells took up iodide and this accumulated iodide was discharged by TSH, PGE2 and DBC. TSH-, PGE2- and DBC-stimulated iodide discharge was depressed greatly after chronic exposure to TSH, PGE2 or DBC. This refractoriness of TSH-, PGE2- or DBC-stimulated iodide dishcarge was not specific for each thyroid stimulating substance; previous exposure to TSH, PGE2 or DBC induced refractoriness of TSH-, PGE2- and DBC-stimulated iodide discharge, providing evidence for the existence of refractoriness at the level of cyclic AMP action on iodide discharge. When incubated with Nal in the absence of MMI, the cells took up iodide and organified it. After 30 min incubation with Nal, TSH, PGE2 and DBC were added and they stimulated iodide organification further. This TSH-, and PGE2-stimulated iodide organification was also depressed after exposure to TSH or PGE2. These data indicate that, as an intrinsic regulatory mechanism, refractoriness is operating at the level of cAMP action on iodine discharge and organification.

Water and electrolyte contents, cell pH and membrane potentials of cultured turtle thyroid cells

1985 ◽  
Vol 104 (1) ◽  
pp. 45-52 ◽  
Author(s):  
S. Y. Chow ◽  
Y. C. Yen-Chow ◽  
D. M. Woodbury
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Culture Medium ◽  
Resting Membrane Potential ◽  
Follicular Cells ◽  
Iodide Uptake ◽  
Thyroid Cells ◽  
Cell Ph ◽  
Cells Cultured ◽  
In Cells

ABSTRACT Water and electrolyte contents, cell pH, membrane potential and 125I− uptake were determined in cultured follicular cells of turtle thyroid. The Na+, K+ and Cl− concentrations in the cultured thyroid cells were 59·2, 119·0 and 50·9 mmol/l cell water respectively. Treatment with TSH (10 mu./ml for 24 h) increased the K+ and Cl− and decreased the Na+ concentrations in cells. The water and protein contents of these cells were 81·6 and 8·7 g/100 g cells respectively. The cell pH was 6·91. With glass microelectrodes, the resting membrane potential of thyroid cells cultured in Medium 199 averaged 33·9 ± 0·63 mV which is slightly higher than 29·8 ± 1·6 mV as calculated from the data on the uptakes of [14C]methyltriphenylphosphonium and 3H2O by the cells. The potential varied linearly with the log of external K + concentration (between 15 and 120 mmol/l) with a slope of about 24 mV per tenfold change in K+ concentration. Both TSH and cyclic AMP depolarized the cell membrane. Calculations based on the values for the electrolyte concentrations in cells and in culture medium indicated that Na+, K+ and Cl− were not distributed according to their electrochemical gradients across the cell membrane. Na+ was actively transported out of the cells and K+ and Cl− into the cells. Follicular cells of turtle thyroid cultured in the medium without addition of TSH formed a monolayer. Their iodide-concentrating ability was low and they did not respond to TSH with an increase in iodide uptake. In contrast, cells cultured in medium containing TSH tended to aggregate and organize to form follicles. They had higher ability to concentrate iodide and respond to TSH. J. Endocr. (1985) 104, 45–52

Voltage-dependent effects of isoproterenol on cytosolic Ca concentration in rat heart

1987 ◽  
Vol 252 (4) ◽  
pp. H697-H703 ◽  
Author(s):  
S. S. Sheu ◽  
V. K. Sharma ◽  
M. Korth
Keyword(s):  
Membrane Potential ◽  
Calcium Concentration ◽  
Ventricular Myocytes ◽  
Cytosolic Calcium ◽  
Resting Membrane Potential ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Agonist ◽  
Voltage Dependent ◽  
K Concentration ◽  
Ca2 Channels

The effect of the beta-adrenoceptor agonist, isoproterenol, on cytosolic calcium concentration ([Ca2+]i) was studied with the Ca2+-sensitive fluorescent indicator quin 2 in enzymatically dissociated rat ventricular myocytes. Under conditions in which cells have normal polarized resting membrane potential, isoproterenol (1 microM) produced a decrease in [Ca2+]i. In contrast, in the depolarized cells (by raising extracellular K+ concentration to 50 mM), isoproterenol (1 microM) caused an increase in [Ca2+]i. This isoproterenol-induced increase in [Ca2+]i in depolarized cells could be reversed by prior exposure of the cells to the Ca2+ channel blocker, verapamil (5 microM). The results indicate that isoproterenol can either decrease or increase [Ca2+]i depending on membrane potential. The actual effect of isoproterenol on [Ca2+]i at any given membrane potential probably reflects the relative contributions of isoproterenol-induced stimulation of Ca2+ buffering or effluxing activities (which favor a decrease in [Ca2+]i) and enhancement of Ca2+ influx through voltage-sensitive Ca2+ channels (which favors an increase in [Ca2+]i).

Responses In Vitro of Human Thyroid Cells to Thyrotrophin and Dibutyryl Cyclic amp

1976 ◽  
Vol 50 (2) ◽  
pp. 29P-30P
Author(s):  
S. P. Bidey ◽  
P. Marsden ◽  
C. G. McKerron ◽  
J. Anderson
Keyword(s):  
Cyclic Amp ◽  
Human Thyroid ◽  
Dibutyryl Cyclic Amp ◽  
Thyroid Cells
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